Embryology - User contributions [en-gb]

User:Z5015337

2016-10-30T08:34:28Z

Z5015337:

{{ANAT2341Student2016}}
==Lab 1 Assessment==
<pubmed>26446757</pubmed>

In the aforementioned research article, the "Onobrychis Viciifolia" or rather, sanfoin is explored in detail with respect to its ability to self fertilise and therefore be a sustainable and useful plant for its local ecosystem. This is due to its ability to reduce the need of nitrogen fixation by bacteria as a Legume. On top of this, Sanfoin has tannins in it that assist with the break down of proteins and as such, it is beneficial to animals.

This research article utilises naturally directed pollination and artificially directed pollination to compare rates of self fertilisation. Interestingly, the plants of sanfoin that used artificially directed pollination had much higher rates of self fertilisation than the natural counterpart. Whilst there are other results obtained, these are the main results that by implication indicate that we can assist the growth of local plant systems by artifically pollinating sanfoin, which will provide nutrients and reduce the dependence on nitrogen fixation for plants to obtain nitrogen.

{| width=95%
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| [mailto:m.hill@unsw.edu.au Mark Hill] 18 August 2016 - You have added the citation correctly and written a good brief summary of the article findings. However, a plant study on "fertilisation" is not really what I was asking, in particular as this is not a Botany course, please try and focus on course content.

| width=100px| Assessment 4/5
|}
==Lab 2 Assessment==
[[User:Z8600021|Mark Hill]] ([[User talk:Z8600021|talk]]) 10:17, 19 August 2016 (AEST) you need to use the full file name (.jpeg).

[[File:Extracellular calcium levels compared to Spermatozoa levels.jpeg]]

Effect of extracellular Ca2+ depletion on the human zona pellucida-induced intracellular [Ca2+] increase in spermatozoa<ref><pubmed>PMC1712232</pubmed>
[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1712232/]</ref>

{| width=95%
|-bgcolor="FAF5FF"
| [mailto:m.hill@unsw.edu.au Mark Hill] 29 August 2016 - All information Reference, Copyright and Student Image template not included with the file and citation not referenced on your page here. I cannot complete the assessment without knowing the original source (reference for this image). Please update so that I can complete the assessment.

| Assessment ??
|}
===Lab 3 Assessment===
{| width=95%
|-bgcolor="FAF5FF"
| [mailto:m.hill@unsw.edu.au Mark Hill] 29 August 2016 - Quiz Mesoderm and Neural

| Assessment 5/5
|}

===Lab 4 Assessment===
====Gastrointestinal Tract Developmen====
.

<quiz display=simple>

{The mesoderm consists of epithelium, connective tissues, blood vessels, mesentry, smooth muscle.
| type="()"}
-   true
+   false
|| Whilst the mesoderm consists of connective tissues, blood vessels, mesentry and smooth muscle, epithelium is located in the endoderm and not the mesoderm .





{Select the most correct option of the following options:
|type="()"}
-   The superior mesenteric artery supplies the hindgut
-   The foregut is suppled by the inferior mesenteric artery
-   The celiac artery supplies the midgut
+   The superior mesenteric artery supplies the midgut
||The superior mesenteric artery supplies the midgut, the celiac artery supplies the foregut and the inferior mesenteric artery supplies the hindgut.



{Which of the following statements about lumen abnormalities are correct:
|type="[]"}
-   Atresia is a term that refers to the narrowing of the lumen
+   The formation of parallel lumens is a form of stenosis
+   An abnormality that results in interruption of the lumen is Atresia
-   Duplication results in perpendicular lumen
|| The key to solving these sorts of questions are to ensure that the questions are read carefully as there is usually a trick in the wording. Atresia refers to an interruption of the lumen, not narrowing of the lumen. Parallel lumen formation is a form of specialized stenosis. As mentioned prior, Atresia refers to an interruption of the lumen. Duplication will result in the formation of parallel lumens and not perpendicular lumens.

{Select the most correct option of the following options in the context of patterning signals:
|type="()"}
-   Endothelin is expressed in the anterior part of the primitive gut.
-   Cdx2 regulates the migration of enteric neural tube cells
+   GDNF regulates the migration of enteric neural crest cells
-   Sox2 is expressed in the posterior part of the primitive gut.

||Endothelin regulates the migration of enteric neural crest cells/ Cdx2 regulates the migration of enteric neural CREST cells, not tube. GDNF regulates the migration of enteric neural crest cells. Sox2 is expressed in the ANTERIOR part of the primitive gut.

</quiz>

{| width=95%
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| [mailto:m.hill@unsw.edu.au Mark Hill] 13 October 2016 - These are good quiz questions, in particular I like your detailed answers. Note that question 4 is a seriously difficult GIT question, as it would require a detailed knowledge of molecular controls.
| Assessment 5/5
|}

==Lab 5 Assessment==
I have completed the prescribed questionnaire during lab.
{| width=95%
|-bgcolor="FAF5FF"
| [mailto:m.hill@unsw.edu.au Mark Hill] 23 September 2016 - Questionnaire on course structure.
| Assessment 5/5
|}

==Lab 6 Assessment==
1. A known genetic mutation that is associated with cleft lip is the mutation of the p63 or TP63 which allows the encoding of the Tumour protein p63.

2. A research article that explores this gene is:

<pubmed>2564545</pubmed>

3. Mutations of the p63 gene are detrimental as it is a critical regulator that prevents a host of defects in development, such as ectodermal dysplasia. Without the presence of this gene in mice, the mice died at birth and had truncated limbs as well as epidermal defects<ref><pubmed>16524929</pubmed>[http://www.ncbi.nlm.nih.gov/pubmed/16524929]</ref>.

In the context of cleft palate syndrome and the p63 gene, there is not a clear reason as to why mutations of the p63 gene can result in cleft palate but as cleft palate is a form of ectodermal dysplasia and functioning p63 prevents dysplasia, a connection can be made <ref>[https://ghr.nlm.nih.gov/gene/TP63#conditions]</ref>.

{| width=95%
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| [mailto:m.hill@unsw.edu.au Mark Hill] 13 October 2016 - These are good brief answers. Question 2 the PMID 2564545 appears to be incorrect as it does not reference a p63 paper? see also [http://www.omim.org/entry/603273?search=p63&highlight=p63 OMIM p63]
| Assessment 4/5
|}

==Lab Attendance==
[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]]) 9/09

[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]])23/09[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]])

==Lab 7 Assessment==
1. The dystrophin gene is located on the locus of the X chromosome and is responsible for the transcription of dystrophin. A mutation of this gene will therefore result in altered expression of the muscle isoform, dystrophin<ref><pubmed>14636778</pubmed></ref> . Mutations like these can result in Autosomal recessive muscular dystrophy and Duchenne and Becker muscular dystrophies to name a few.

2. Dystrophin is a critical protein that is responsible for linking the actin filaments to the sarcolemma, which is a protein that is located in the interior of the plasma membrane of individual muscle fibres<ref><pubmed>11917091</pubmed></ref>. Dystrophin is critical in ensuring the stability of muscle fibres and without it intracellular calcium handling is altered resulting in muscular function being impaired<ref><pubmed>15470384 </pubmed></ref>.

3. Other organs that are affected by this disorder are the heart and those responsible for respiration as there is gradual loss of healthy muscular fibres which by cellular repair mechanisms are replaced with inelastic fibrous tissue resulting in less effective contractions resulting in cardiac and respiratory failure<ref><pubmed>4767260</pubmed></ref> .

4.

5 The animal models available for muscular dystrophy are historically the MDX mouse and more recently, a canine DMD.<ref><pubmed> 25740330</pubmed> [https://www.ncbi.nlm.nih.gov/pubmed/25740330]</ref>

{| width=95%
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| [mailto:m.hill@unsw.edu.au Mark Hill] 13 October 2016 - You have answered all the questions except 4? What therapies exist for DMD? While there are no existing cures, there are a number of known therapies, such as corticosteroids for suppression of the associated inflammation in the muscles.
| Assessment 4/5
|}

==Lab 8==
{| width=95%
|-bgcolor="FAF5FF"
| [mailto:m.hill@unsw.edu.au Mark Hill] 27 October 2016 - Urogenital paper quiz - Q1 - Sry acts on testes support cells. Q5 theca and interstitial. Q 8 not all options selected.
| Assessment 5.5/8
|}

==Lab 9 Assessment==
'''Group 1 Review'''

You guys have done really well to accumulate a lot of relevant information so far on your wiki page which is definitely a positive for your team. In the context of criterion 1 of the assessment criteria, I am not certain that the key points are clearly described as of yet, there is just a lot of information that is not presented to the reader in a targeted manner, so this definitely needs some work. As I have stated previously the choice of content appears to be adequate to address your topic however you guys need to work on increasing the number of subheadings as well as providing an introduction as the project aims remain unclear. Content is not completely correctly referenced yet, presumably due to the fact that you guys are still making your project page up but referencing is very easy to do correctly on this wiki and I implore you to make sure it is done correctly when it is time to submit the assignment.

As I have alluded to previously, elements of teaching at a peer level were completely missing in this and these definitely need to be addressed, probably by putting entries into your glossary as well as creating a well structured introduction. It would also help if you guys drew some representations of information, such as sketches of pathways. There is certainly evidence of going above and beyond the formal learning activities, which is a major positive for your project. In the context of learning objectives of the course, you guys are addressing the aspect of embryological development but have not addressed the relevance of new technologies in the WnT Pathway.

Overall, there is a lot of potential for you guys to put out a very good wiki page if you clean up your page so that it is more coherent and insert some information that is lacking so that a relatively uneducated reader could understand the WnT signalling pathway from the wiki page. Well done!

'''Group 2 Review'''

At first glance, I was blown away by your team's page. Definitely very impressive and understandable. The key points relating to the Notch signalling process are definitely clearly described however I may recall Dr Hill requesting that teams steer clear of clinical effects of genes(citation needed!). The choice of headings, sub-headings and diagrams show more than a good understanding of the topic area, it may be useful to include a table that summarises the various aspects of the Notch pathway so that readers realise there are different receptors. The content is cited correctly, however, I would not mind reading 'et al' instead of 'and colleagues' more often, I got sick of reading 'and colleagues'.

The information presented is mostly peer friendly in the context of a simple introduction but your glossary certainly needs updating, there are a lot of terms that a lot of students would not understand and a comprehensive checking of your page will offer you a list of words that you need to define. Also lacking are sketches presented in your own hands, instead of reusing published images. There is plenty of evidence that suggests your team has went beyond the formal teaching activities. In the context of the aims of the embryology course, you guys have emphasised the embryonic role of Notch but the aspect of developing technologies appears to have been ignored to an extent.

Overall, you guys have done a very impressive job that only requires minor tweaking, namely slight editing in the context of in text referencing, more comprehensive glossary as well as checking the course aims of embryology to incorporate the second criterion regarding technology. Excellent work!

'''Group 4 Review'''

Nice effort group 4. Key points that relate to the Hedgehog signalling pathway are very succinctly described. Your choice of headings, albeit brief, provides a sense that you guys understand the topic generally but I feel as if you could improve on your subheadings, for example of the Clinical Significances section, I feel as if the diagnosis subheading could be altered. I also feel as if the information in the Organogenesis section could be reworked into an introduction which would allow you to then focus on Organogenesis on its own in more detail. Also, you guys only have one image so far which seems to be slightly lacklustre, you guys definitely need more images. The relevant content is mostly cited correctly, albeit the odd reference located below the marking criteria, I feel as if that is more of a small accident.

The information presented is relatively peer friendly. Perhaps more explanation, for example in the Processing of precursor section as I felt well and truly lost in that area. You guys could do with some hand drawn diagrams or analogies to help explain the information provided. A glossary section would be very helpful in understanding the wiki page, by defining the complex terms such as proteasome(which is misspelt on your page as proteosome). The research that has been done has indicated that you guys have went beyond the formal teaching activities, however, you guys could do more research in the sections that have no information for example 'History', you could even put a timeline in there! In the context of the course aims, he embryological relevance of the Hedgehog pathway is addressed to an extent but as you have missing sections under human disease, there is still work to be done in this section. Also, you should try to complete your current research section to address the second criterion of the course aims regarding new technologies and research.

Overall you guys have had a good start and really just need to start filling in the blanks so to speak. Your team researches information well, just ensure that you fill in your missing sections and think of innovative ways to present information. Nice job!

'''Group 5'''

Your team has a very impressive wiki page, well done! The key points relating to T-Box as well as your choice of subheadings and headings are very good, however I would advise removing 'Good places to look'. In terms of diagrams, tables and graphs, these are present and augment the information presented quite well. The content presented is cited mostly correctly however care must be taken with pictures, which have to be checked for copyright reuse as well as ensuring that they are cited correctly in the first place, I would advise that your team checks each of your pictures to make sure that they are correctly cited.

In the context of peer level education, your content is understandable and written well even though the topic is complex. What is lacking however are using your own explanations as well as interesting hand drawn visual stimuli to present information, this can be easily remedied. Also, completion of the glossary section so that someone can understand complex terms would be useful. With the information that has been provided and the depth of research that has went into the meticulous presentation of information regarding T-box, it is clear that your team has went beyond formal teaching activities, however, perhaps the inclusion of some interactive features on your page such as a video with voice over or a quiz would help augment this criterion. The learning aims of the Embryology course are mostly in line with the information on the wiki page, but there is no section for current research/technologies, which is important to address the second criteria of the course aims.

Overall, you guys did a very nice job that requires only minor touch ups and the addition of a few pieces of information. Don't forget the current research section though, that is pretty important to include in my opinion. Well done!

'''Group 6'''

Good try group 6. Key points appear to be well selected, however perhaps consideration of clinical aspects of your research could be considered useful. Your subheadings should be fixed so that all of your information does not come under the introduction section and also perhaps include more pictures in your project. You guys have a good lay out of information, now you really just need to fill those sections up with information, definitely have a sound understanding of the topic area. There are little to no references as of yet and none of the references in the references section have been cited correctly, this can be fixed by simply using the inbuilt referencing mechanism we have been using for our weekly assessment items. Also, more peer reviewed journal articles should be used and cited to provide authority to your information.

The information presented is very peer friendly and understandable but will need the inclusion of hand drawn diagrams to satisfy this criterion completely. There is not much evidence to suggest that your team has went beyond the formal teaching activities, perhaps incorporate a video or quiz into your work. In terms of the course aims of embryology, you have not satisfied the second criteria regarding new technology/current research as of yet and have vaguely addressed the key criteria regarding TGF and embryological development.

Overall, the areas to be discussed appear to be sound but need to be edited so that the information will flow better. Your team needs to put more information into each section, I would recommend looking at some of the other teams to see how much information is seemingly adequate. Ensure that you reference your information correctly and you should be good when you guys put more research onto your page. Good luck and nice
try!

{{Stem Cell Presentations 2016}}

==Lab 12 Assessment==
Foglia and Poss (2016) have written a review article that describes the process of cardiac tissue regeneration and development. Its primary focus is comparing the regeneration of cardiac muscle after myocardial infarction(heart attack) in humans and animals and why the healing is different.

One of the primary research articles cited by Foglia and Poss explored how D-type cyclins promote cardiomyocyte cell cycle activity(Pasumarthi et al, 2004). By causing myocardial injury to mice which had either cyclin D1,D2 or D3 production promoted, they observed that the synthesis of the cardiomyocyte DNA was affected. Hence, their main finding was that the mice with enhanced cyclin D2 had increased cardiomyocyte DNA synthesis whereas the mice with enhanced D1 or D3 did not. In summary, their primary finding is that cardiomyocyte cell cycle activity persisted in D2 mice but not D1 or D3<ref><pubmed>15576649 </pubmed></ref>. However, in the context of Foglia and Poss'(2016) review paper, this paper was used to provide evidence that D2 can stimulate cardiocyocyte DNA synthesis. It should be acknowledged that the review paper also notes D1 as performing the same role as D2 even though the primary paper by Pasumarthi et al. (2004) found the opposite true. The review paper will have used the other primary papers referenced to prove that cyclins D1 as well as D2 stimulate cardiomyocyte DNA synthesis.

==New Sub-Heading==
===External Link===
===Internal Link===
https://embryology.med.unsw.edu.au/embryology/index.php/ANAT2341_Lab_1
===References===
[http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=fertilization fertilization]

2016 Group Project 3

2016-10-27T12:15:39Z

Z5015337: /* External Genitalia development */

{{ANAT2341Project2016header}}
{{Group Assessment Criteria table}}


=Fibroblast Growth Factor Receptor (FGFR) Pathway=
==Introduction==
The Fibroblast Growth Factor (FGF) signalling pathway is critical for regulating progenitor cell proliferation, differentiation, survival and patterning. It is involved in the regulation and development of the early embryo, and is considered to be critical for normal vascular, skeletal and organ development. Furthermore, this pathway is involved in maintaining adult tissues through the regulation of metabolic functions and tissue repair (which is often through the reactivation of the same signalling pathways involved in early development.) <ref name="PMID25772309"><pubmed>25772309</pubmed></ref>

This page will outline the FGFR signalling pathway, the history of scientific discoveries relevant to this pathway, receptor sub-types and a description of signal transduction. It will also describe its various roles in embryonic development including its influence on the patterning of the embryonic axis, as well as limb bud, bone, kidney, external genitalia and inner ear development. There is also a discussion of relevant animals models, such as those of the chick embryo, as well as abnormalities in this pathway relevant to embryonic development, including Achondroplasia, Pfeiffer syndrome and Apert syndrome. A short informative quiz accompanied with feedback is offered for readers to determine how much they have learnt from the information provided. A glossary at the bottom of the page explains specific terms mentioned throughout, along with links to relevant information from UNSW embryology lectures.

===History===
Ranging from its discovery in 1939 till the present, much has been learned about the nature of Fibroblast growth factor (FGF) in embryonic development. Researchers had noticed the growth stimulating effects that these isolated factors had, in that they induced fibroblast proliferation. Due to their ability to stimulate fibroblast proliferation they were termed "FGFs". Today, a variety of subtypes of FGFs have been discovered and categorised into a large family that exist in organisms including humans as well as nematodes. In addition, it was soon discovered that not all FGFs can stimulate fibroblasts.

The table below outlines some of the significant scientific discoveries regarding the FGFR signalling pathway over the years, as outlined in a review article. <ref><pubmed>26793421</pubmed></ref>

{| class="pretty table"
|-bgcolor = "DDCEF2"
|'''Year'''
|'''Scientific Discovery Regarding FGF/FGFR Signalling'''
|-bgcolor="FAF5FF"
| '''1939'''
|The first paper on FGFs was published through experiments that measured the mitogenic activity of saline extracts of different tissues from the chick. Early work also investigated the idea that uncontrolled proliferation is a hallmark of cancers and the involvement of growth factors such as FGF.
|-
|'''1974
|FGF growth factor activity was shown to stimulate the growth of a fibroblast cell line in partially purified extracts from bovine pituitary. This lead to the term "fibroblast growth factor" to be derived.
|-bgcolor="FAF5FF"
|'''1987'''
| The interaction with heparin that FGFs have was translated into work regarding the interaction of FGFs with the glycosaminoglycan heparan sulfate within the pericellular and extracellular matrix.
|-
|'''1989'''
| FGF1 and FGF2 were isolated from brain tissue.
|-bgcolor="FAF5FF"
|'''1990'''
|FGFR tyrosine kinases were identified for the first time
|-
|'''1991'''
| FGFs were also shown to display growth factor activities on fibroblasts. In addition, the dependence of the growth factor activity of FGFs on heparan sulfate was discovered.
|-bgcolor="FAF5FF"
|'''2005'''
|A further set of FGF proteins termed the FGF homology factors were found to be wholly intracellular such that they do not interact with any of the extracellular receptors and partners of FGFs.
|-
|'''2013'''
|A small group of FGFs were found to not bind heparan sulfate, but instead to interact with a protein co-receptor named Klotho.
|-
|}

=== Overview Of The FGFR Pathway===
23 protein families have been identified from the FGF signalling pathway, 18 of which are secreted signalling proteins (FGF1-10, and FGF16-23) that interact with 4 tyrosine kinase FGF Receptors (FGFR1-4), whilst 4 are intracellular non-signalling proteins (iFGFs; FGF11-14). <ref name="PMID25772309"/>

As illustrated in the image below, FGFRs are comprised of 3 immunoglobulin domains (IgI, IgII, IgIII), with IgIII being the closest to the transmembrane and IgI being the furthest away. Some notable features of this receptor include an acidic box (AD) located in-between IgI and IgII, a heparin-binding domain (HBD) within IgII which is important in signal transduction, and the transmembrane (TM) structure of IgIII which has both kinase and interkinase domains (KD and IKD) within the intracellular space. FGF ligands linked to heparin sulfate proteoglycan (HSPG) bind to both the IgII and IgIII domain of the receptor (with the heparin component specifically binding to IgII) resulting in dimerisation of the receptors and activation of signal transduction pathways through the phosphorylation of tyrosine residues, as discussed in more detail under the subheading signal transduction. <ref><pubmed>16216232</pubmed>[http://www.ncbi.nlm.nih.gov/pubmed/16216232]</ref>

[[File:FGFR receptor subtype.jpeg|thumb|none|300px|Simplistic illustration of the FGFR receptors adapted from review article [http://www.ncbi.nlm.nih.gov/pubmed/16216232 Functions and regulations of fibroblast growth factor signaling during embryonic development]]]

===Subtypes of FGFR===
{| class="pretty table"
|-bgcolor="DDCEF2"
| '''FGFR Subtype''' || '''Function''' || '''Abnormalities'''
|-bgcolor="FAF5FF"
| FGFR1 ||
*Involved in morphogenesis as well as orchestrating the patterning of the mesodermal germ layer at gastrulation<ref><pubmed>16207751</pubmed></ref> 
*Involved in formation of the organ of corti and auditory sensory epithelium <ref><pubmed>12194867</pubmed></ref> 
*Expressed in early limb bud <ref><pubmed>1321062</pubmed></ref> 
*Expressed at epiphyseal growth plate as well as in the perichondrium, prehypertrophic and hypertrophic chondrocytes<ref><pubmed>17169623 </pubmed></ref> 
*Is a negative regulator of bone growth<ref><pubmed>16815385</pubmed></ref> 
||
*Pfeiffer Syndrome (Type 1)
*Kallmann syndrome
*Osteoglophonic dysplasia
*8p11 myeloproliferative syndrome

|-
| FGFR2 ||
*Activated prior to gastrulation with the purpose of repressing cellular movements in the presumptive anterior neural plate and preventing normal retinal progenitor cells from adopting retinal fates<ref><pubmed>14723847</pubmed></ref> 
*Acts as a marker of prechondrogenic condensations<ref><pubmed>9784595</pubmed></ref> 
*Expressed in condensing mesenchyme of the early limb bud<ref><pubmed>1315677</pubmed></ref> 
*Plays a key role in skeleton development as it is expressed in osteoprogenitor cells and differentiating osteoblasts<ref><pubmed>20489451 </pubmed></ref> 
*Is involved in cranial cell replication or differentiation in both humans and mice.<ref><pubmed>15863034 </pubmed></ref> 
||
*Pfeiffer Syndrome (Type 1-3)
*Apert Syndrome
*Crouzon Syndrome
*Beare-Stevenson cutis gryata syndrome<ref><pubmed>17552943 </pubmed></ref> 
|-bgcolor="FAF5FF"
| FGFR3 ||
*Induces complete growth arrest of cells<ref><pubmed>11779141 </pubmed></ref> 
*Is required to promote differentiation of prechondrogenic mesenchymal cells to cartilage-producing chondrocytes <ref><pubmed>8432397 </pubmed></ref> 
*Is expressed in chondrocytes, differentiated initially from the core of the mesenchyme condensation<ref><pubmed>8630492 </pubmed></ref> 
*Is expressed in reserve and proliferating chondrocytes as the epiphyseal growth plate is formed<ref name="PMID 12080084"><pubmed>12080084</pubmed></ref> 
||
*Achondroplasia (can be severe, with developmental delay and acanthuses)
*Thanatophoric Dysplasia
*Hypochondroplasia
|-
| FGFR4 ||
*Involved in proliferation of the blastocyst inner cell mass, differentiation of the presomitic mesoderm and limb bud development<ref name ="PMID 10662638"><pubmed>10662638</pubmed></ref> 
*Regulates cholesterol metabolism, bile acid synthesis and liver mineral homeostasis
*It will provide mitogenic and morphogenic signals to regulate normal limb development<ref name="PMID 12080084"/> 
*Promotes intramembranous ossification and participates in the development of calvarial bone<ref name ="PMID 10662638"/> 
||
*Chondrodysplasia
|-
|}

===Signal Transduction===
 [[File:FGF signalling pathway.jpg|thumb|500px|FGFR Signalling Pathway (Image based upon<ref><pubmed>27458533</pubmed></ref>)]]

The process of signal transduction commences with the binding of a cognate ligand to FGFRs ligand binding site which in turn triggers receptor dimerization. This dimerization of the receptor will cause activation of intrinsic kinase activity<ref><pubmed>1655404</pubmed></ref>. This will activate multiple signal transduction pathways intracellularly including RAS, Mitogen-activated protein kinase (MAPK), p38 MAPKs, Phospholipase-C-Gamma, Crk, Protein Kinase-C and Phospholipase-C-Gamma and Extracellular signal-regulated kinases. Activation of FGFRs induces tyrosine phosphorylation of FRS2 (FGFR stimulated2 Grb2 binding protein) which in turn stimulates the recruitment of GRB2 (Growth factor receptor bound protein-2) and SHP2 ( Src homology 2 phosphatase-2) <ref><pubmed>11021964</pubmed></ref>.
 
 
In turn, this sequence of events promotes sustained activation of RAS, which leads to changes in gene transcription through interactions with DNA. In addition, FGF receptors will also induce the activation of PI3K (phosphatidylinositol-3-Kinase), STAT1 and Src tyrosine kinase, which will contribute to certain FGF-stimulated biological responses <ref><pubmed>1656221</pubmed></ref>.
 
 
With respect to embryonic development, both the PI3K and RAS pathways are essential in order for the normal mesoderm to develop in the embryo. Additionally, receptor-mediated induction of the SHP2-RAS-ERK pathway is a key mechanism through which FGF can activate a variety of biological signalling pathways including cell growth, cellular differentiation as well as morphogenesis <ref><pubmed>9632781</pubmed></ref>.

{| class="wikitable mw-collapsible mw-collapsed"
! YouTube video outlining FGF Signalling Pathway
|-
|<html5media height="400" width="533">https://www.youtube.com/watch?v=DUBelRjjqvc</html5media>
 
This is a YouTube animation which illustrates a simplified version of the FGF Signalling pathway discussed above. This signalling pathway leads to changes to gene expression that, for example, can result in changes in cell growth, division or differentiation.<ref> Oxford University Press (2015, March 9) the FGF Signalling Pathway [Video file]. Retrieved from https://www.youtube.com/watch?v=DUBelRjjqvc </ref>
|}

==Role In Embryonic Development==

===Patterning Of The Embryonic Axis===
In the process of patterning of the embryonic axis, the caudal primordium that is part of the neural plate, contains cells that are rapidly dividing and is able to maintain itself as a growth region (this region is considered to be of "stem cell" status). The expanding populations of dividing cells spread along the neural tube by cell movements of convergence and extension. As cells undergo a process whereby they are driven out of the tube, they change their pattern of movement, which eventually causes a gradual restriction in space<ref><pubmed>8575335</pubmed></ref>. Within this process, it is the misexpression of a dominant negative FGFR construct in the tissue which causes these cells to prematurely leave the stem cell region and to change their movement patterns as if they had aged<ref><pubmed>11389440</pubmed></ref>.

Furthermore, Mathias et al. (2001) suggest that FGFR is required in order to maintain this stem cell status in the caudal neural plate during patterning of the nervous system. In addition, it is possible that FGF serves the purpose of acting as a caudalizing factor for the neural tube because it is capable of prolonging the window of time during which cells are exposed to a caudalizing factor.

In summary, FGF signalling is important in regulating the maturation of developing cells which are gradually being laid down in a caudal direction along the axis of the neural tube.

===Limb Bud Formation===
[[File:LIMB BUD.png|200px|thumb|400px|Mechanisms of FGF signalling during organises; a-c: limb development, d-e: lung development, f-h: induction of the otic placode and differentiation of the otic vesicle<ref name="PMID25772309"/>]]

Limb buds are structures formed early in [[Lecture - Limb Development| limb development]] which are comprised of lateral plate mesoderm (LPM) cells and an overlying surface ectoderm. They are roughly formed around week 4 of embryonic development as a result of interactions between the mesoderm and ectoderm germ layers.

FGF proteins and its interactions with other signalling pathways, are critical for the initiation and proximal-distal growth of limbs from a limb bud structure.<ref><pubmed>9620845</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/9620845]</ref> The following information is accompanied by a YouTube video below and the image on the right, where figures a-c corresponds specifically to limb bud formation<ref name="PMID25772309"/> Prior to limb bud formation, FGF10 is widely expressed in the LPM and is stabilized by the WNT signaling proteins. FGF10 is responsible for stimulating the expression of WNT3 (and downstream transcription factors including SP6 and SP8<ref><pubmed>15358670</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/15358670]</ref>) in the overlying ectoderm, which results in the formation of the Apical Ectodermal Ridge (AER), a specialised thickening of epithelium located towards the proximal end of the bud that is required for growth,<ref name="PMID25772309"/> which subsequently stimulates FGF8. FGF8 is responsible for continued growth of the underlying mesoderm by keeping it in a mitotically active state, and stimulating a positive feedback loop on FGF10 (which in turn stimulates increased FGF8 expression). FGF8 is the known AER-specific FGF to be expressed throughout it, although other FGFs are expressed in the posterior AER (including Fgf4, Fgf9 and Fgf17) and are thought to have supporting roles.<ref><pubmed>11101846</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/11101846]</ref><ref><pubmed>12152071</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/12152071]</ref>
FGFs in the AER signal FGFR1 and FGR2 in distal mesenchyme, activating ETV1 and EWSR1 which function to help to maintain FGF10 expression.<ref><pubmed>25109552</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/25109552]</ref>

Furthermore, the Zone of Polarising Activity (ZPA) is a region located on the posterior side of the limb bud composed of mesenchyme which signals its anterior-posterior growth (for example this region signals the position of the thumb relative to the little finger.) The Fibroblast Growth Factors FGF2<ref><pubmed>7908145</pubmed> [https://www.ncbi.nlm.nih.gov/pubmed/7908145]</ref>, FGF4<ref><pubmed>8001146</pubmed> [https://www.ncbi.nlm.nih.gov/pubmed/8001146]</ref> and FGF8<ref><pubmed> 8598907</pubmed> [https://www.ncbi.nlm.nih.gov/pubmed/8598907]</ref> induce Sonic Hedgehog (SHH) within ZPA region and is critical for its growth along the anterior-posterior axis.

Therefore together these interactions of the FGFs from the AER help to maintain proliferating cells near the distal tip of the limb bud, and are known to be critical in limb bud development, both along the proximal-distal axis and the anterior-posterior axis. It is also important to note that growth along the dorsal-vental axis is dependent on the involvement of growth factors from the Wnt family on the ectodermal layer.

FGF signaling is also involved in lung bud initiation and development, with a similar underlying process.This is supported by the accompanying image on the right, where figures d and e specifically looks at the interplay of FGFs and FGFRs on the lung bud imitation and lung development.<ref name="PMID25772309"/>

{| class="wikitable mw-collapsible mw-collapsed"
! YouTube video outlining limb bud development
|-
|<html5media height="400" width="533">https://www.youtube.com/watch?v=VpbdqGJ9LWk</html5media>
 
YouTube video outlining limb bud development<ref>Itzel García (2012, July 9) Limb development [Video file]. Retrieved from https://www.youtube.com/watch?v=VpbdqGJ9LWk</ref>
|}

===Bone Development===
[[File:FGF and FGFR expression patterns during endochondral and intramembranous bone development.jpeg|thumb|400px|FGF and FGFR expression patterns during endochondral and intramembranous bone development <ref name="PMC4526732"><pubmed>PMC4526732</pubmed>
[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526732/]</ref>]]

Much of what we now understand about the involvement of the FGF signalling pathway in bone development is a result of discovering missense mutations responsible for conditions characterised by abnormal bone structure, including but are not limited to, skeletal dysplasias and craniosysnostosis syndromes (some of which discussed in more detail later under the subheading abnormalities.) The first and questionably the most important mutation discovered affecting skeletal development was a point mutation of the FGFR3 protein, which was found to be responsible for achondroplasia. <ref><pubmed>7913883</pubmed></ref>

FGF signalling is involved in both endochondral and intramembranous [[Lecture - Musculoskeletal Development| bone development]], which are critical in the early stages of embryonic bone formation. As shown in the diagram to the right the presence of FGFR1-3 and FGF2, FGF9, FGF18 are involved in various stages of bone development.

Endochondral bone development (A-D in the figure) is responsible for forming the long bones of the appendicular skeleton, face and spinal column. This involves an intermediate cartilage template (which helps control the growth and patterning of the development of the bony structure.) As shown in the figure provided by a review article<ref name="PMC4526732"/> FGFR signalling is present across different stages of development (ranging from mesenchymal condensation to the establishment of the primary ossification centre. FGFR2 (light blue) expression is prominent in mesenchymal condensation, FGFR1 (white) is uniformly expressed throughout the mesenchyme, and both FGFR3 (red) and FGFR4 (not shown) are not present in distal limb bud mesenchyme and expressed proximally in tissues related to developing muscle. <ref><pubmed>21302260</pubmed></ref> In comparison, intramembranous bone development (G in the figure) is responsible for forming bones of the skull and clavicles, and doesn’t require a cartilage template, it directly forms bone. As shown in the figure provided by a review article<ref name="PMC4526732"/> we primarily see the presence of FGFR1 (white) on mesenchymal cells and both FGFR1 and FGFR2 (dark blue) on osteoprogenitor cells, osteoblasts and osteocytes (in mineralised bone.) Furthermore, this figure also shows FGF and FGFRs involvement in both the Embryonic (E in the figure) and Postnatal Growth Plate (F in the figure) and highlights how they are distributed differently between these two stages of life.<ref name="PMC4526732"/>

For additional information see the recent (2015) review article by Ornitz1 and Pierre [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526732/ ''Fibroblast growth factor signaling in skeletal development and disease'']

===Kidney development===
The metanephric kidney is an organ which arises primarily form two tissues, the nephrogenic cord and the Wolffian duct, which will eventually give rise to the metanephric mesenchyme and the ureteric bud respectively <ref><pubmed>18835385</pubmed></ref>. Around week 5 of gestation in the developing human embryo, the metanephric mesenchyme will release signalling molecules that stimulate the ureteric bud to grow out from the Wolffian duct and invade the metanephric mesenchyme. The stromal mesenchyme that exists between the Wolffian duct and the metanephric mesenchyme restricts the ureteric bud to its proper position and prevents ectopic budding<ref><pubmed>10749566</pubmed></ref>. The metanephric mesenchyme will continue to release signals which will stimulate the ureteric bud to elongate and repeatedly branch, leading to formation of the ureter, collecting duct system and the renal pelvis. Following its contact with the ureteric bud, the metanephric mesenchyme will then divide into a nephrogenic lineage lying adjacent to the bud, and a surrounding renal cortical stromal lineage <ref name="PMID19272374"><pubmed>19272374</pubmed></ref>. Each terminal tip of the ureteric bud induces local areas of nephrogenic mesenchyme in order to differentiate into nephron epithelia, progressing from renal vesicles ,to comma-shaped bodies, to S-shaped bodies, and then to immature nephrons<ref name="PMID19272374"/>. The renal cortical stroma will provide a framework and likely a niche for the other renal lineages and vasculature, and ultimately differentiates into interstitial and other supportive cells within the kidney <ref><pubmed>10594778</pubmed></ref>.

In terms of the development of the metanephric kidney, all FGFRs have been detected in the process of development, however studies using animal models have revealed that it is FGFR1, FGFR2 and FGFR11 which play a key role in renal development <ref><pubmed>10691305</pubmed></ref>. FGFR1 is a receptor which is expressed mostly in the metanephric mesenchyme lineages, these including the early metanephric mesenchyme, the cap mesenchyme and the developing nephrons beginning with vesicles. However, FGFR1 is present at lower levels in the ureteric lineage and in the renal cortical stroma<ref><pubmed>10385628</pubmed></ref>. In contrast, FGFR2 is strongly expressed in the Wolffian duct and the ureteric bud tree as well as the differentiating nephrons. Despite this, FGFR2 is present at lower levels in the early metanephric mesenchyme and stomal mesenchyme adjacent to the Wolffian duct<ref name="PMID1315677"><pubmed>1315677</pubmed></ref>. In addition, FGFR11 is present in renal vesicles <ref name="PMID1315677"/>.

===External Genitalia development===
[[File:External genitalia.jpg|thumb|200px|External genitalia development<ref><pubmed>26081573</pubmed></ref>]]
The genital tubercle (GT) is a structure from which characteristics in the external genitalia in the adult develop. The GT differentiates into a penis in males and a clitoris in females. The process of proximodistal elongation of this GT involves multiple interactions between growth factors and transcription factors <ref><pubmed>3723059</pubmed></ref>. Interactions between epithelium and mesenchyme have an essential role in the regulation of various development processes throughout the embryo. Such signalling controls many aspects of organogenesis, from the initiation of organ development to differentiation <ref><pubmed>8896986</pubmed></ref>.

The FGFR signalling pathway is involved in epithelial to mesenchymal interactions during organogenesis. Studies have revealed that the first morphological sign of GT outgrowth occurs at approximately 10.5 days post coitum, and will continue throughout the perinatal period <ref><pubmed>12004962</pubmed></ref>. Initially within the developing embryo, the external genitalia of the male and female foetuses are morphologically identical and consist of the GT. Several growth factors including FGF proteins have been shown to control external genitalia development in mice <ref><pubmed>10021340</pubmed></ref>. FGF8, FGF10 and FGFR2 expression has been found during GT developing, thus suggesting that a combination of these factors may constitute redundant developmental functions during GT morphogenesis<ref><pubmed>10804187</pubmed></ref>. As the GT elongates, a groove appears on its ventral aspect called the urethral groove. At the distal end, this groove is made up of a solid plate of epithelial cells, the distal urethral epithelium (DUE) that extends into the glans penis. The solid urethral plate canalizes and thus extends the urethral groove distally into the glans. It was found that FGFR2IIIb is expressed in the DUE and urethral plate epithelia of the GT. Deletion of this receptor and FGF10 was shown to cause urethral dysmorphogenesis.

It was also shown that the deletion of FGR2 or FGF10 would result in hypospadias in mice, where when FGFR2 was deleted in the ectoderm leads to severe hypospadias and absence of the ventral prepuce whereas when FGFR2 was deleted in the endoderm, mild hyospadias occurs and maturation of complex urethral epithelium was inhibited<ref><pubmed>26081573 </pubmed></ref>. Specifically, in female mice, it was shown that those mice with severe hypospadias had a single urogenital opening and in a particular group of these mice, the tip of the urethral plate was separated from the vaginal orifice. These results indicates that FGFR2 action mediates urethral epithelial maturation and FGFR2 in the ectoderm is responsible for the formation of prepuce.

===Inner ear development===
[[File:Inner ear development.jpg|500px|thumb|Inner ear development (Image was retrieved from a review article<ref><pubmed>22855724 </pubmed></ref>]]
The inner ear, containing the vestibule and cochlea, is derived from a simple ectodermal thickening called the otic placode. Genetic evidence and expression of data has lead to the suggestion that FGF3 and other fibroblast growth factor types influence early development of the mammalian inner ear, specifically by regulating the formation of the endolymphatic duct <ref><pubmed> 12761848</pubmed></ref>. FGFR-3 is expressed in the cochlear special sensory epithelium, particularly during late embryogenesis and during postnatal life. To reinforce this, further investigations have revealed that FGFR3 absence leads to deafness attributable to disturbances in the differentiation of the cochlear sensory epithelium<ref><pubmed> 8630492</pubmed></ref>. Studies have also revealed that cochlear neuron-derived FGF1 and inner hair cell-derived FGF8 may serve as ligands which bind to FGFR-3 during the late embryonic and postnatal cochlea. In addition, FGF9 mRNA has been localised to the otic vesicle and to the later developing nonsensory epithelium and ganglion of the cochlea<ref><pubmed> 10474167</pubmed></ref>.
 
 
In studies which investigated the dynamic expression patterns of FGF10 and FGFR-2 mRNAs, it was revealed that FGF10 was widely expressed in the undifferentiated otic epithelium however it was subsequently restricted to the presumptive cochlear and vestibular sensory patches. Also, the strong expression of FGF10 mRNAs was found in the otic epithelium-derived neuronal precursors and in the neurons of the cochleovestibular ganglion. Furthermore, te expression of FGF10 mRNA and its colocalization with neurotrophin mRNAs in the ventral patch is indicative that neurons belonging to the inner ear as well as part of the sensory epithelium, have a common origin in this epithelial domain<ref><pubmed> 8071140</pubmed></ref>. In the cranial nerve ganglion, FGF10 mRNA was found within those of the cochlear and vestibular ganglia and not in the surrounding ganglia, which is suggestive that FGF10 relates to the unique colocalization of neurotrophin receptors in the inner ear sensory neurons. Alternative studies have revealed that hindbrain-derived FGF3 has been suggested to regulate patterning of the inner ear, particularly the endolymphatic duct <ref><pubmed>8223243</pubmed></ref>. It was further revealed that FGF3 mRNA is expressed in the ventrolateral region of the otic vesicle at the same stage that it is visible in the hindbrain.

==Animal Models==
===Mouse Models===
Over the past few decades, extensive studies in mice have yielded insights into the roles of various FGF molecules and signalling pathways in embryonic development. In particular, loss-of-function genetic analysis in the mouse has been crucial for understanding FGF function. <ref name ="PMID26666435"><pubmed>26666435</pubmed></ref>

For example, one of the most recent models developed for studying Fgf functions during development, as reported in Genesis in February 2016, is the Fgf3(Δ)-Fgf4(flox)-cis mouse line <ref name="PMID26666435"/>. This model newly allows exploration of redundancy between Fgf3 and Fgf4 genes which are both located on chromosome 7, 18.5 kb apart, by retargeting Fgf3 and Fgf4 in cis, generating an Fgf3 null allele and a conditional Fgf4 allele subject to Cre inactivation. The line showed caudal axis extension defects in Fgf3 mutants to worsen with Fgf4 inactivation, demonstrating redundancy. The model can be applied in the future study redundancy of these genes in a variety of tissues and stages of development.

The following table summarises selected mouse models with germline, conditional or temporarily induced knockout or deficiency for specific FGFs that have been used to certain demonstrate defective aspects of embryological development. Many of these mouse models continue to be used in emerging medical research into the respective pathologies they characterise.
{| class="pretty table"
|-bgcolor="DDCEF2"
| '''Mouse Type''' || '''Phenotype expressed''' || '''Viability in Null Mutant'''
|-bgcolor="FAF5FF"
| Fgf1-, Fgf21- ||
*impaired energy/lipid metabolism, diabetes under high-fat diet<ref><pubmed>22522926</pubmed></ref> <ref><pubmed>23874946</pubmed></ref> 
||
Viable
|-
| Fgf2- ||
*decreased vascular muscle contractility, low blood pressure, thrombocytosis <ref><pubmed>9461194</pubmed></ref> 
*decreased cardiac hypertrophy in ischaemic injury <ref><pubmed>10491406</pubmed></ref> 
*reduced cortical neurogenesis <ref name="PMID 9576942"><pubmed>9576942</pubmed></ref> 
*reduced skin wound healing <ref name="PMID 9576942"/> 
*reduced trabecular bone formation <ref><pubmed>10772653</pubmed></ref>, dwarfism, rickets, osteomalacia <ref><pubmed>25389287</pubmed></ref> 
||
Viable
|-bgcolor="FAF5FF"
| Fgf3- ||
*defective inner ear <ref><pubmed>8223243</pubmed></ref> 
*defective heart <ref name ="PMID21664901"><pubmed>21664901</pubmed></ref> 
||
E15.5 <ref name ="PMID21664901"/> 
|-
| Fgf4- ||
* impaired blastocyst inner cell mass proliferation <ref name="PMID 7809630"><pubmed>7809630</pubmed></ref> 
||
E4-4 <ref name="PMID 7809630"/> 
|-bgcolor="FAF5FF"
| Fgf7- ||
* impaired ureteric bud development, decreased number of nephrons <ref name ="PMID 9876183"><pubmed>9876183</pubmed></ref> 
* prone to seizures <ref><pubmed>20505669</pubmed></ref> 
||
Viable <ref name ="PMID 9876183"/> 
|-
| Fgf8- ||
* failed gastrulation <ref><pubmed>10421635</pubmed></ref> 
* defective kidney development <ref><pubmed>16049111</pubmed></ref> 
* defective limb development <ref><pubmed>11101846</pubmed></ref> 
* defective inner ear <ref><pubmed>15741321</pubmed></ref> 
* defective cerebellum <ref><pubmed>10751172</pubmed></ref> 
* defective heart outflow tract <ref><pubmed>14975726</pubmed></ref> 
||
E7 <ref><pubmed>10421635</pubmed></ref> 
|-bgcolor="FAF5FF"
| Fgf9- ||
* lung hypoplasia <ref><pubmed>16540513</pubmed></ref> 
* male to female sex reversal <ref><pubmed>11290325</pubmed></ref> 
* rhizomelia <ref><pubmed>17544391</pubmed></ref> 
* shortened small intestine <ref>pubmed>18653563</pubmed></ref> 
* cecal agenesis <ref><pubmed>22819677</pubmed></ref> 
* cardiomyopathy <ref name="PMID 15621532"><pubmed>15621532</pubmed></ref> 
* ataxia <ref><pubmed>19232523</pubmed></ref> 
||
P0 <ref><pubmed>11493531</pubmed></ref> 
||
|-
| Fgf10- ||
* lung hypoplasia <ref name="PMID9784490"><pubmed>9784490</pubmed></ref> 
* defective limb development <ref name="PMID9784490"/> 
* defective inner ear formation <ref><pubmed>14623822</pubmed></ref> 
* defective pancreatic development <ref><pubmed>12810586</pubmed></ref> submandibular salivary gland <ref><pubmed>15972105</pubmed></ref> and defective mammary gland <ref><pubmed>16720875</pubmed></ref> 
* defective tracheal cartilage <ref><pubmed>21148187</pubmed></ref> and cleft palate <ref><pubmed>15199404</pubmed></ref> 
* cecal agenesis <ref><pubmed>22819677</pubmed></ref> 
||
P0 <ref name="PMID9784490"/> 
|-bgcolor="FAF5FF"
| Fgf 13- ||
* impaired learning memory and neuronal excitability, neuronal migration defects <ref><pubmed>22726441</pubmed></ref> 
||
Viable
|-
| Fgf14- ||
* impaired learning, memory and neuronal excitability <ref name="PMID 17236779"><pubmed>17236779</pubmed></ref> 
* ataxia <ref><pubmed>12123606</pubmed></ref> and motor weakness <ref name="PMID 17236779"/> 
||
Viable
|-bgcolor="FAF5FF"
| Fgf15- ||
* Heart defects in outflow tract <ref><pubmed>15789410</pubmed></ref> 
* neurogenesis <ref><pubmed>18625063</pubmed></ref> 
* bile acid metabolism <ref><pubmed>16213224</pubmed></ref> 
||
E13.5-P7 <ref><pubmed>15789410</pubmed></ref> 
|-
| Fgf16- ||
* cardiomyopathy <ref name="PMID 15621532"/> 
||
Viable
|-bgcolor="FAF5FF"
| Fgf17- ||
* defective cerebellum <ref><pubmed>10751172</pubmed></ref> and frontal cortex <ref><pubmed>17442747</pubmed></ref> 
||
Viable
|-
| Fgf18- ||
* lung development defects <ref name="PMID 15336546"><pubmed>15336546</pubmed></ref> <ref><pubmed>11927601</pubmed></ref> 
* bone and cartilage development defects <ref><pubmed>26595272</pubmed></ref> 
||
P0 <ref name="PMID 15336546"/> 
|-bgcolor="FAF5FF"
| Fgf20- ||
* kidney agenesis <ref><pubmed>22698282</pubmed></ref> 
* cardiomyopathy <ref name="PMID 15621532"/> 
||
Viable <ref name="PMID 15621532"/> 
|-
| Fgf23- ||
* deafness, defective middle ear development <ref><pubmed>25243481</pubmed></ref> 
* hyperphosphatemia and impaired vitamin D metabolism <ref name="PMID 14966565"><pubmed>14966565</pubmed></ref> 
||
PW12 <ref name="PMID 14966565"/>
|-
|}

===The Importance of FGF10 in Limb and Lung Development in Chicks and Mice===
[[File:Mice model and limb development.gif|thumb|400px|Mice model and limb development<ref name="PMID9784490"/>]]
In vertebrate embryos, initiation of limb buds results from the outward proliferation of the lateral plate mesoderm<ref><pubmed> 9323126</pubmed></ref>. The distal ectoderm surrounding this region is then induced by dividing mesenchymal cells to thicken and form a structure called the apical ectodermal ridge (AER). Molecular interactions that occur between the AER and the underlying mesenchyme are vital in order for proximal-distal patterning to occur. FGF2, 4 and 8 are expressed in the AER of Chicks, and are capable of replacing the AER to induce underlying mesenchyme to maintain its distal outgrowth. The anterior-posterior patterning of each limb bud is regulated by the zone of polarizing activity (ZPA), which is located at the posterior margin of the limb bud mesenchyme<ref name="PMID4826292"><pubmed> 4826292</pubmed></ref>.

Tissue graft experiments have indicated that vertebrate limb bud formation is initiated by factors from mesoderm within the limb field<ref name="PMID4826292"/>. Implantation of beds soaked in FGFs or FGF-expressing cells is capable of inducing formation of ectopic limbs within chick embryos. FGF 1, 2, 4, 8 and 10 were shown to exhbit limb-inducing activity<ref><pubmed> 7889567</pubmed></ref>. However, only FGF8 and FGF10 will express demonstrate the correct temporal and spatial expression that could guide the initiation of the limb bud. FGF8 in chick embryos is expressed in the intermediate mesoderm at presumptive limb regions before limb bud initiation. This is compared to FGF10, which is only expressed in the lateral plate mesoderm within the limb field prior to limb bud initiation, and the expression persists in the mesenchyme under AER after initial limb bud formation<ref><pubmed> 8674413</pubmed></ref>.

Evidence also suggests that FGF10 may also affect development of the vertebrate lung. In mice, the process of lung morphogenesis begins with ventral extension of the laryngotracheal groove from the primitive gut endoderm approximately at E9.5. After this stage, the tracheal primordium will bifurcate to produce left and right principal bronchi, around which the lung buds differentiate. Further branching of these bronchi result in the development of bronchioles and alveoli that form mature lung parenchyma. A recent study suggests that an FGF-mediated signal plays a major role in lung development. A splice variant of FGFR2 is highly expressed in respiratory epithelium during early branching morphogenesis in the epithelium of the respiratory tract during early branching morphogenesis<ref><pubmed> 15632068</pubmed></ref>.In further investigations, when FGF10 was absent in the developing embryos of mice, there was complete absence of budding limbs at E9.5 whilst all other external structures remained. Thus these results suggest that FGF10 is necessary for limb bud initiation<ref name= "PMID9784490"/>.
 

==Abnormalities==
As discussed above, the FGF signalling pathway is critical for regulating many early embryonic developmental processes, and is critical for normal organ, vascular and skeletal development. Consequently, abnormalities in genes coding for the proteins within this signalling pathway (including signalling proteins, non-signalling proteins, and receptors) can result in many visible structural abnormalities such as short statue and face deformations. Not to mention that a large majority of these conditions, if not all, influence an individual’s quality of life, and in some cases increase risk of fatality. Some of these FGF abnormalities are outlined in more detail below, including Achondroplasia, Pfeiffer and Apert Syndrome which particularly emphasise the significance of FGF signalling in early skeletal development.

===Achondroplasia===
Achondroplasia is the most common form of skeletal dysplasia, and is often characterised by shortened proximal limbs, a curved spine, a large prominent forehead and a fattened nasal bridge. This condition is inherited genetically as an autosomal dominant trait, although a large proportion of cases are sporadic. <ref><pubmed>7913883</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/7913883]</ref> This condition results in reduced inhibition of endochondral ossification, which is one of the main way in which bone tissue is created during embryonic development (the other being intramembranous ossification.) Endochondral ossification is essential during development for both the formation and growth of long bones as well as healing fractures. For the majority of affected individuals, it is a result of a missense mutation in FGFR3, specifically due to a substitution of arginine for glycine (G380R).<ref><pubmed>12816345</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/12816345]</ref> As originally postulated by Bonaventure et al. (1996) this introduction of a hydrophilic residue in a hydrophobic receptor domain results in a disruption of alpha-helical structure of the transmembrane portion of the protein and consequently interferes with the signal transduction pathway of which it is involved in. <ref><pubmed>8723101</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/8723101]</ref>

There are other mutations in FGFR3 which are responsible for different skeletal developmental conditions, including a more severe (usually fatal) form of skeletal dysplasia, Thanatophoric Dysplasia, which is due to two different mutations, K650E and R248C in FGFR3 (type 1 and type 2 respectively) and a milder form, hypochondroplasia, which is due to the mutations, N540K or K650N in FGFR3. Recent studies have also shown expression of an fgf4 retrogene to be associated with achondroplasia in domestic dogs. <ref><pubmed>19608863 </pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/19608863]</ref>

===Pfeiffer Syndrome===
Pfeiffer syndrome is characterised by craniosynostosis, meaning that is it a condition where the cranial fibrous sutures prematurely fuse (ossify) resulting in a reduced space for the growing brain. Subsequently, abnormal growth of the skull, in an attempt to increase the space available for the brain and reduce cranial pressure, results in the development of abnormal facial features including, but not limited to, proptosis (abnormal placement of the eye), hypertelorism (abnormal increase in distance between the eyes), maxillary deficiency, and a beaked nose. Other notable features include those of the hands, broad thumbs and the feet, medially deviated broad great toes.
<ref><pubmed>9300656</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/9300656]</ref><ref name= "PMID25679016"><pubmed>25679016</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/25679016]</ref> This condition is inherited genetically as an autosomal dominant trait. There are 3 types of Pfeiffer syndrome. Type 1 is a result of either a gain of function P252R mutation of FGFR1 (5%), which increases the receptor’s ligand binding affinity resulting in over-activation of the receptor, or sequence variants of FGFR2 gene (95%.)<ref name= "PMID25679016"/> Type 2 and 3 are similar, both appear more severe and generally have a worse prognosis compared to Type 1, and are a result of mutations of the FGFR2 gene.
<ref><pubmed>8434615</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/8434615]</ref><ref><pubmed>10394936</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/10394936]</ref>

{| class="wikitable mw-collapsible mw-collapsed"
! YouTube video outlining Pfeiffer Sydrome
|-
|<html5media height="400" width="533">https://www.youtube.com/watch?v=UKYcDm2QHtU</html5media>
 
YouTube video outlining Pfeiffer Sydrome<ref>wyscrvr (2011, March 23) Pfeiffer Syndrome [Video file]. Retrieved from https://www.youtube.com/watch?v=UKYcDm2QHtU</ref>
|}

===Apert Syndrome===
[[File:Syndactyly.jpg|thumb|200px| Syndactyly of the fingers]]
Apert syndrome is characterised by craniosynostosis, as well as turribrachycephaly (high, prominent forehead), midface hypoplasia (incomplete/underdevelopment) and syndactyly (cutaneous and bony fusion) of the fingers and toes. This condition is inherited genetically as an autosomal dominant trait. It is a result of a gain-of-function mutation of FGFR2, specifically at S252W or P253R region, which is responsible for increased receptor affinity for the binding ligand and subsequently result in excessive activation of the receptor. <ref><pubmed>26220993</pubmed></ref><ref name= "PMID25679016"/> It is currently thought that the P253R mutation will increase the affinity of FGFR2 to all FGFs, whereas the S252W mutation on the other hand will increase the affinity of FGFR2 only to a selective subset of FGFs. <ref><pubmed>11390973</pubmed></ref> The genotype of the mutation is thought to explain clinical variability in the presentation of the condition in patients. <ref name= "PMID25679016"/>

===Additional Information Regarding Abnormalities in FGFR Signalling===
The abnormalities regarding the FGFR signalling pathways that have been discussed above are widely researched and reported on. However, there are many more conditions resulting from mutations in the FGFR signalling pathway and always ongoing research into these conditions in which it causes. For more information regarding the conditions mentioned above, and in general abnormalities of FGFR signalling, links to OMIM have been provided below.

{{About OMIM}}
Conditions Mentioned Above:
* [http://omim.org/entry/100800 Achondroplasia]
* [http://omim.org/entry/101600 Pfeiffer Syndrome]
* [http://omim.org/entry/101200 Apert Syndrome]

Fibroblast Growth Factor Receptor Subtypes:
* [http://www.omim.org/entry/136350 Fibroblast Growth Factor Receptor 1]
* [http://www.omim.org/entry/176943 Fibroblast Growth Factor Receptor 2]
* [http://www.omim.org/entry/134934 Fibroblast Growth Factor Receptor 3]
* [http://www.omim.org/entry/134935 Fibroblast Growth Factor Receptor 4]

===FGF and FGFR Abnormalities in Cancer===
Deregulation of FGF signaling pathways have been implicated in many types of human and animal cancers <ref name= "PMID25772309"/>. This deregulation can be heritable or acquired during development or postnatally.

These abnormalities in signalling may arise from mutations in genes for FGF ligands, receptors, or downstream signaling pathways, as well as modified protein or gene expression of ligands or receptors at the transcriptional level or via gene amplification. Mechanisms of FGF ligand activation include aberrant expression and gene amplification leading to ligand overexpression, resulting in excessive FGF signaling. Secondary mutations that increase diffusion of FGFs through tissue or increase affinity for FGFRs may also contribute. FGFRs can also be activated by mutations, gene amplification leading to receptor overexpression, or by translocations resulting in activating fusions with adjacent genes. Activation of FGFRs by somatic acquisition of missense mutations is another common tumorigenic mechanism. Each of these mechanisms ultimately results in cancer initiation or progression.

Recent advancements in understanding these pathogenic mechanisms in FGFs and FGFRs has led to therapeutic approaches for a variety of cancers. <ref><pubmed>23696246</pubmed></ref>

The following table describes the types of FGF and FGFR genetic mutations associated with numerous of the most common cancers in humans and their prevalence.

{| class="pretty table"
|-bgcolor="DDCEF2"
| '''Carcinoma Type''' || '''FGF/FGFRs Associated''' || '''% Affected (if known)'''
|-bgcolor="FAF5FF"
| Bladder ||
*over expression of FGF2 <ref><pubmed>20299037</pubmed></ref>
*amplification, translocation and missense mutation in FGFR3 <ref><pubmed>17255960</pubmed></ref> <ref><pubmed>23175443</pubmed></ref>
||
*FGFR3 was amplified in 3% <ref><pubmed>24898159</pubmed></ref>
*missense mutations in FGFR3 have been observed in 35% <ref><pubmed>10471491</pubmed></ref>
|-
| Breast ||
*amplification of FGF3 and FGF4, over expression of FGF8 <ref><pubmed>11953856</pubmed></ref> <ref><pubmed>10023681</pubmed></ref> and FGF10 <ref><pubmed>15208658</pubmed></ref>
*amplification of FGFR1 and FGFR2 <ref name = "PMID 23270564"><pubmed>23270564</pubmed></ref>, over expression and missense mutation in FGFR3 <ref><pubmed>11329138</pubmed></ref>, missense mutation in FGFR4 <ref><pubmed>16822847</pubmed></ref>
||
*FGFR1 amplification identified in 20% lobular breast cancer <ref name = "PMID 23270564"/>
*FGFR4 amplification found in 10% primary breast tumors <ref><pubmed>8099571</pubmed></ref>
|-bgcolor="FAF5FF"
| Colorectal ||
*amplification and missense mutation in FGFR2 and FGFR3 <ref><pubmed>11325814</pubmed></ref>
*missense mutation in FGFR4 <ref name ="PMID 20844967"><pubmed>20844967</pubmed></ref>
||
*FGFR4 mutation present in 57% of patients <ref name ="PMID 20844967"/>
|-
| Glioblastoma ||
* over expression of FGF5 <ref><pubmed>18362893</pubmed></ref>
* over expression and translocation of FGFR1, translocation of FGFR3 <ref><pubmed>22837387</pubmed></ref>
||
* 3.1% exhibit FGFR1 or FGFR3 mutation
|-bgcolor="FAF5FF"
| Hepatocellular ||
* over expression of FGF2 <ref><pubmed>15836707</pubmed></ref>, FGF8 <ref><pubmed>21319186</pubmed></ref>, FGF15/19 <ref><pubmed>22309595</pubmed></ref>, FGF17, FGF18 <ref><pubmed>21319186</pubmed></ref>
* over expression of FGFR4 <ref><pubmed>25031272</pubmed></ref>
|-
| Leukemia & Lymphoma ||
* translocation of FGFR1 <ref><pubmed>9425908</pubmed></ref>
||
|-bgcolor="FAF5FF"
|Lung Adenocarcenoma ||
*over expression of FGF7 <ref><pubmed>15307144</pubmed></ref> and FGF9 <ref><pubmed>23867472</pubmed></ref> <ref><pubmed>25413587</pubmed></ref>
*FGFR1 amplification <ref name = "PMID21666749"><pubmed>21666749</pubmed></ref>
||
*FGFR1 amplification identified in 3% <ref name = "PMID21666749"/>
|-
|Lung Squamous Cell ||
*amplification of FGFR1 <ref><pubmed>24302556</pubmed></ref>
*translocation of FGFR3 <ref><pubmed>23661334</pubmed></ref>
||
*FGFR1 amplification identified in 21-28% cases <ref><pubmed>21160078</pubmed></ref> <ref><pubmed>24302556</pubmed></ref>
|-bgcolor="FAF5FF"
|Lung Small Cell||
* over expression of FGF2 <ref><pubmed>11165400</pubmed></ref>
* amplification of FGFR1 <ref name= "PMID 24294370"><pubmed>24294370</pubmed></ref>
||
*43.7% exhibit FGFR1 amplification, with worse prognostic outcomes <ref name= "PMID 24294370"/>
|-
| Lung Non-Small Cell||
*over expression FGF9 <ref name="PMID 24239165"><pubmed>24239165</pubmed></ref>
||
*10%, with 3-fold increase in likelihood of post-operative occurrence<ref name="PMID 24239165"/>
|-bgcolor="FAF5FF"
| Melanoma <ref><pubmed>8311116</pubmed></ref> ||
*over expression of FGF2
*missense mutation and amplification of FGFR1
||
|-
|Ovarian||
*amplification of FGF1 <ref><pubmed>17538174</pubmed></ref>, overexpression FGF16 <ref><pubmed>24253043</pubmed></ref>
*amplification of FGFR1, over expression of FGFR4 <ref><pubmed>16822847</pubmed></ref> <ref><pubmed>23344261</pubmed></ref>
||
|-bgcolor="FAF5FF"
|Pancreatic ||
* amplification of FGFR1 <ref><pubmed>12105858</pubmed></ref>
||
* 2.6-4% <ref><pubmed>23808822</pubmed></ref>
|-
|Prostate||
*over expression of FGF2 <ref><pubmed>23243019</pubmed></ref>, FGF6 <ref><pubmed>10945637</pubmed></ref>, FGF8 <ref><pubmed>12778074</pubmed></ref>, FGF10 <ref><pubmed>18068633</pubmed></ref>, FGF15/19 <ref><pubmed>23440425</pubmed></ref>, FGF17 <ref><pubmed>15129425</pubmed></ref>, polymorphism in FGF23 <ref><pubmed>24053368</pubmed></ref>
*amplification of FGFR1 and FGFR2 <ref name="PMID14614009"><pubmed>14614009</pubmed></ref>
||
*FGFR1 or FGFR2 was amplified in 47% of hormone resistant prostate cancers <ref name="PMID14614009"/>
|-
|}

==Quiz: How much do you really know about FGF? Take the quiz and find out!==

<quiz display=simple>

{ How many FGFRs have been discussed in this page?
|type="()"}
- 1
+ 4
- 18
- 22
|| Observing the table of the different types of FGFRs that have been discovered it is clear that there are four types of FGFRs. Thus, option B is the correct answer.

{ Which of the following describes FGFR as a receptor type?
|type="()"}
- G-protein coupled receptor
+ Tyrosine kinase receptor
- Electrically coupled receptor
- None of the above
|| FGFR are a tyrosine kinase receptor type. Thus meaning, the binding of an extracellular ligand will induce receptor dimerization. This process will allow a tyrosine in the cytoplasmic portion of the receptor to be trans-phosphorylated by its adjacent receptor, which in turn induces a signal through the plasma membrane. Thus option B is the correct.

{ Which of the following statements are true?
|type="()"}
- FGFR attaches at the outer surface of the lipid bilayer
- FGFR attaches on inner surface of lipid bilayer
+ FGFR cross the membrane and is thus transmembrane
- Options A and B
|| Upon observing the illustration of FGFR at the beginning of this page, it is clear that the receptor itself will traverse the lipid bilayer of the cell. Thus option C is correct.

{ Which of the following statements regarding FGFR3 is true?
|type="()"}
- Mutation in the receptor causes Pfeiffer Syndrome
+ Induces complete growth arrest of cells
- Prevents chondrocytes from developing
- Associated with Kallmann syndrome
|| FGFR3 has many roles ranging from its role in promoting differentiation of prechondrogenic mesenchymal cells to cartilage thus producing chondrocytes to inducing complete growth arrest of cells. This will mean that cell growth will come to a complete hault. Thus option B is correct.

{ Which of the following molecules will directly bind to the DNA in the final stages of the signal transduction pathway?
|type="()"}
+ATF2 and Elk1
-FAS2 and Raf1
-PLD and Rac1
-PKC and IP3
|| Signalling molecules which bind the DNA molecule are capable of altering gene expression within the cell. In the process of FGFR signalling, the two molecules which do this are ATF2 and Elk1, thus the correct answer is A.

{Which of the following statements are correct?
|type="()"}
-The use of an anti-FGFR3 antibody for treatment in skeletal-related disorders has no risk of side-effects or toxicity
+ Genetic inactivation of ERK1 and ERK2 in chondrocytes can promote enlargement of the spinal canal
- Genetic activation of ERK1 only can cause apoptosis of cells within the spinal canal
-ERK1 has been proven to inhibit the formation of chondrocytes in the process of bone growth
|| In a study, it was revealed that when ERK1 and ERK2 in chondrocytes are inactivated, this can promote the enlargement of the spinal canal as well as promote the process by which bone develops. Thus the correct answer is B

{ Regarding lung small cell cancer, one which is very aggressive, abnormalities in FGF signalling have been demonstrated in the pathogenesis of this disease. In the process:
|type="()"}
-FGF2 is underexpressed
-FGFR1 is reduced significantly
+FGF2 is over expressed
-FGF9 is over expressed
||Lung small cell cancer is a type of cancer that has the ability to metastasise at very early stages which is why it is considered to be deadly. In studies discussed in the above table which links FGF abnormalities to disease, it has been revealed that over expression of FGF2 is an event that occurs in small cell carcinoma. Thus option C is correct.
</quiz>

==New and emerging research surrounding FGFRs==
===Promising therapeutic methods to alleviate the skeletal phenotypes resulting from dysfunction FGFs/FGFRs===
[[File:Bone signalling pathway1.gif|thumb|400px|Signals regulating bone growth]]
A variety of studies have been conducted in order to investigate methods that will alleviate the skeletal phenotypes caused by dysfunctional FGFs/FGFRs signalling. In gain of function mutations, the major strategy of treatment is to reduce their excessive activities, subsequently alleviating the impaired cell functions, whilst in contrast, loss of function mutations or deficiency are treated by supplementation of related factors <ref><pubmed>15310757</pubmed></ref>.
 
 
In order to prevent excessive intracellular signalling and to alleviate the symptoms of FGFs and FGFR-related genetic disorders, a variety of molecules targeting FGFRs or their tyrosine kinase were used. A soluble form of the Apert mutant, FGFR2, which lacked the transmembrane and cytoplasmic domains, will compete for ligand binding with FGFRs, thus enhancing the process of osteoblastic differentiation of cells in the osteosarcoma cell line transfected with the Apert mutant. Recently, it was found that FGFR2 may partially prevent craniosynostosis in the Apert mouse model <ref><pubmed>17694057</pubmed></ref>. There has also been an increase in the number of studies related to FGFR3-related skeleton disorders. A31, which is a tyrosine kinase inhibitor, is a capable of restoring normal expression of cell cycle regulators and allow pre-hypertonic chondrocytes to properly differentiate into hypertonic chondrocytes in cultured femurs from achondroplasia (ACH) mice<ref><pubmed>22072392</pubmed></ref>. In addition, further research has been able to develop a recombinant protein therapeutic approach which uses a soluble form of FGFR3, as a decoy receptor, in order to rescue the phenotype of ACH transgenic mice with no toxicity<ref><pubmed>24048522</pubmed></ref>. Another approach to target FGFR3 is to use an anti-FGFR3 antibody, however the antibody may carry a risk of an antibody-dependent cell cytotoxic reaction, which prevents its use in ACH.
 
 
Studies have also demonstrated that ERK, a molecule downstream of the FGFR signalling pathway, is responsible for retarded growth of long bones and premature fusion of the synchondroses caused by abnormal FGFR3 expression<ref name= "PMID9069288"><pubmed> 9069288</pubmed></ref>. Genetic inactivation of ERK1 and ERK2 in chondrocytes can promote the enlargement of the spinal canal and promote bone growth. From another study it was found that inhibition of ERK signalling may enlarge the narrowing of the spinal canal, thus alleviating neurological complications of ACH. <ref name= "PMID9069288"/>.

 
 
 

===Emerging Research Into The Role Of FGF In The Development Of The Growth Plate===
https://www.ncbi.nlm.nih.gov/pubmed/25114206
 
===Autoregulatory loop of induction between FGF10 and FGF8 ===
 
 

FGFR2 is a membrane spanning receptor that acts as a receptor for members of the fibroblast growth factor family. By mutating the FGFR2 in mice, a number of novel findings were determined regarding the importance of this receptor <ref><pubmed>9435295</pubmed></ref>. None of the embryos with mutated FGFR2’s survived due to the resulting developmental deficits from a dysfunctional FGFR2. Furthermore, induction of FGF8 is blocked in the limb ectoderm and the expression of FGF10 in the underlying mesoderm is reduced. This highlights the importance of the FGFR2 receptor as well as indicating its involvement in a signalling loop between FGF8 and FGF10. Due to the functions of FGF8 and FGF10, it has been postulated that interaction between these two FGF members is imperative for limb bud formation, in the context of the epithelial – mesenchymal interaction.

Whilst the role of FGFR2 has been described in the context of FGF8 and FGF10, it is important to acknowledge that there are many other pathways that use these fibroblast growth factors and interrupting these will result in similarly disastrous issues. For example, by inhibiting B – catenin activity, limbs will become truncated, indicating FGF-10 being affected and FGF8 expression in the ectoderm was severely down regulated<ref><pubmed>11290326</pubmed></ref>. This shows how the signalling loop between FGF8 and FGF10 can be affected in many different ways and in this instance, by altering the amount of B – Catenin available to the embryo.

== Further Information Regarding FGFR Signalling and Embryology==

{| class="wikitable mw-collapsible mw-collapsed"
! Recent Papers From PubMed
|-
|{{Most_Recent_Refs}}
Search term: ''FGF Signalling In Organogenesis''

<pubmed limit=5>FGF Signalling In Organogenesis</pubmed>
|}
{| class="wikitable mw-collapsible mw-collapsed"

 
 
 

 

==Glossary==
Glossary definitions are sourced from lectures presented in the UNSW embryology course ANAT2341 (in addition to the glossary provided online in the course, which is linked to at the bottom of these selected terms which are related to this page.)
{| class="pretty table"
|-bgcolor="DDCEF2"
|'''Term'''
|'''Definition'''
|-bgcolor="FAF5FF"
|'''Animal Models'''
|Is a term used to describe animals studies that are used in research, they may have either an existing, inbred or induced disease/injury (that can be related to a human condition)
|-
|'''Apical Ectodermal Ridge (AER)'''
|Is a term used to describe the specialised thickening of the epithelium located towards the tip of the limb bud, it is formed by Wnt signalling and secrets FGFs which stimulates proliferation and outgrowth. It acts as a signalling centre ensuring appropriate limb development, including the patterning of the proximal-distal axis of the limb. For more information see [[Musculoskeletal System - Limb Development| Limb Development]]
|-bgcolor="FAF5FF"
|'''Autosomal Dominant Inheritance'''
| A term used to describe the pattern of inheritance whereby one copy of a gene containing a mutation is sufficient to manifest into the disease. For more information see [[Abnormal_Development_-_Genetic#Genetic_Inheritance |Genetic Inheritance]]
|-
|'''Craniosysnostosis Syndromes'''
| Are conditions where the cranial fibrous sutures prematurely fuse (ossify) resulting in a reduced space for the growing brain. The skull compensates for this fusion by growing parallel to the suture, meaning that the skull is abnormally shaped.
|-bgcolor="FAF5FF"
|'''Ectoderm'''
|One of the initial germ cell layers formed during gastrulation (the others being endoderm and mesoderm). It is the outmost layer and is responsible for the formation of the nervous system and the entire epithelial layer of skin covering the embryo. For more information see [[Ectoderm | Ectoderm]]
|-
|'''Endoderm'''
|One of the initial germ cell layers formed during gastrulation (the others being ectoderm and mesoderm). It is the innermost layer and is responsible for the formation epithelial lining of the gastrointestinal and respiratory tract, as well as contributions to the accessory organs of the GIT. For more information see [[Endoderm | Endoderm]]
|-bgcolor="FAF5FF"
|'''Endochondral Ossification'''
| Is one of the two processes that are critical in the early stages of embryonic bone formation. (The other being intramembranous ossification, see below.) This process involves an intermediate cartilage template and is essential for the formation and growth of long bones of the appendicular skeleton, face and spinal column. For more information see [[Lecture - Musculoskeletal Development| Bone Development]]
|-
|'''Fibroblast Growth Factors (FGFs)'''
| Are a family of 22 proteins, 18 of which are secreted signalling proteins (FGF1-10, and FGF16-23) and the other 4 are intracellular non-signalling proteins (iFGFs; FGF11-14)
|-bgcolor="FAF5FF"
|'''Fibroblast Growth Factor Receptors (FGFRs)'''
| Are a family of 4 tyrosine kinase receptors (FGFR1-4) that interact with the signalling FGF proteins
|-
|'''Gastrulation'''
| Is the process whereby the trilaminar embryo formed containing the three germ layers (endoderm, ectoderm and mesoderm). For more information see [[Gastrulation| Gastrulation]]
|-bgcolor="FAF5FF"
|'''Germ Layers'''
| Refers to the three layers: (endoderm, ectoderm, mesoderm) which are primary cell layers from early in embryogenesis, which give rise to all tissues and organs
|-
|'''Intramembranous Ossification'''
| It is one of the two processes that are critical in the early stages of embryonic bone formation. (The other being endochondral ossification, see above.) It directly forms bone, it doesn’t require a cartilage template like endochondral ossification. It is responsible for the formation of bones of the skull and clavicles. For more information see [[Lecture - Musculoskeletal Development| Bone Development]]
|-bgcolor="FAF5FF"
|'''Limb Bud'''
| The initial embryonic structures responsible for the formation of the paired upper and lower limbs. For more information see [[Musculoskeletal System - Limb Development|Limb Development]]
|-
|'''Lung Bud'''
| The initial embryonic structures responsible for the formation of the lungs. For more information see [[Lecture - Respiratory Development | Respiratory Development]]
|-bgcolor="FAF5FF"
|'''Mesenchymal Tissue'''
|(also Mesenchyme) is a term used to describe cellular organisation of undifferentiated embryonic connective tissue, Its contributions include both mesoderm and neural crest, which are responsible for forming most of the adult connective tissue
|-
|'''Mesoderm'''
| One of the initial germ cell layers formed during gastrulation (the others being ectoderm and endoderm). It is the middle layer and is responsible for the formation of all the connective tissue of the body (with the exception of the head region which has additional contributions from the neural crest.) For more information see [[Mesoderm | Mesoderm]]
|-bgcolor="FAF5FF"
|'''Missense Mutations'''
| A point mutation, replacement of a single nucleotide, which results in a different codon (coding for a different amino acid, this is considered to be a type of non-synonymous substitution)
|-
|'''Morphogenesis'''
|Is a term used to describe the process of development involving a change in form (shape)/size of either cells/tissues
|-bgcolor="FAF5FF"
|'''Phenotype'''
|Is a term used to describe the observable characteristics of an organism and is related to the expressed genotype
|-
|'''RAS'''
| A family of related proteins which is expressed in all animal cell lineages and organs.
|-bgcolor="FAF5FF"
|'''Sensory Placode'''
|Is a thickening of surface ectoderm present (paired) in the head region of the early embryo which contribute to a different component of each sensory system (including the otic placode, optic placode, olfactory placode.) For more information see [[Lecture - Sensory Development | Sensory Development]]
|-
|'''Skeletal Dysplasia'''
| A general term that relates to disorders affecting normal bone development
|-
|}

''Below are links to a more extensive glossary if additional definitions are needed''

[[A]] | [[B]] | [[C]] | [[D]] | [[E]] | [[F]] | [[G]] | [[H]] | [[I]] | [[J]] | [[K]] | [[L]] | [[M]] | [[N]] | [[O]] | [[P]] | [[Q]] | [[R]] | [[S]] | [[T]] | [[U]] | [[V]] | [[W]] | [[X]] | [[Y]] | [[Z]]

''Some external links were included throughout this page.''
{{External Links}}

==References==

<references/>

2016 Group Project 3

2016-10-27T11:30:14Z

Z5015337:

{{ANAT2341Project2016header}}
{{Group Assessment Criteria table}}


=Fibroblast Growth Factor Receptor (FGFR) Pathway=
==Introduction==
The Fibroblast Growth Factor (FGF) signalling pathway is critical for regulating progenitor cell proliferation, differentiation, survival and patterning. It is involved in the regulation and development of the early embryo, and is considered to be critical for normal vascular, skeletal and organ development. Furthermore, this pathway is involved in maintaining adult tissues through the regulation of metabolic functions and tissue repair (which is often through the reactivation of the same signalling pathways involved in early development.) <ref name="PMID25772309"><pubmed>25772309</pubmed></ref>

This page will outline the FGFR signalling pathway, the history of scientific discoveries relevant to this pathway, receptor sub-types and a description of signal transduction. It will also describe its various roles in embryonic development including its influence on the patterning of the embryonic axis, as well as limb bud, bone, kidney, external genitalia and inner ear development. There is also a discussion of relevant animals models, such as those of the chick embryo, as well as abnormalities in this pathway relevant to embryonic development, including Achondroplasia, Pfeiffer syndrome and Apert syndrome. A short informative quiz accompanied with feedback is offered for readers to determine how much they have learnt from the information provided. A glossary at the bottom of the page explains specific terms mentioned throughout, along with links to relevant information from UNSW embryology lectures.

===History===
Ranging from its discovery in 1939 till the present, much has been learned about the nature of Fibroblast growth factor (FGF) in embryonic development. Researchers had noticed the growth stimulating effects that these isolated factors had, in that they induced fibroblast proliferation. Due to their ability to stimulate fibroblast proliferation they were termed "FGFs". Today, a variety of subtypes of FGFs have been discovered and categorised into a large family that exist in organisms including humans as well as nematodes. In addition, it was soon discovered that not all FGFs can stimulate fibroblasts.

The table below outlines some of the significant scientific discoveries regarding the FGFR signalling pathway over the years, as outlined in a review article. <ref><pubmed>26793421</pubmed></ref>

{| class="pretty table"
|-bgcolor = "DDCEF2"
|'''Year'''
|'''Scientific Discovery Regarding FGF/FGFR Signalling'''
|-bgcolor="FAF5FF"
| '''1939'''
|The first paper on FGFs was published through experiments that measured the mitogenic activity of saline extracts of different tissues from the chick. Early work also investigated the idea that uncontrolled proliferation is a hallmark of cancers and the involvement of growth factors such as FGF.
|-
|'''1974
|FGF growth factor activity was shown to stimulate the growth of a fibroblast cell line in partially purified extracts from bovine pituitary. This lead to the term "fibroblast growth factor" to be derived.
|-bgcolor="FAF5FF"
|'''1987'''
| The interaction with heparin that FGFs have was translated into work regarding the interaction of FGFs with the glycosaminoglycan heparan sulfate within the pericellular and extracellular matrix.
|-
|'''1989'''
| FGF1 and FGF2 were isolated from brain tissue.
|-bgcolor="FAF5FF"
|'''1990'''
|FGFR tyrosine kinases were identified for the first time
|-
|'''1991'''
| FGFs were also shown to display growth factor activities on fibroblasts. In addition, the dependence of the growth factor activity of FGFs on heparan sulfate was discovered.
|-bgcolor="FAF5FF"
|'''2005'''
|A further set of FGF proteins termed the FGF homology factors were found to be wholly intracellular such that they do not interact with any of the extracellular receptors and partners of FGFs.
|-
|'''2013'''
|A small group of FGFs were found to not bind heparan sulfate, but instead to interact with a protein co-receptor named Klotho.
|-
|}

=== Overview Of The FGFR Pathway===
23 protein families have been identified from the FGF signalling pathway, 18 of which are secreted signalling proteins (FGF1-10, and FGF16-23) that interact with 4 tyrosine kinase FGF Receptors (FGFR1-4), whilst 4 are intracellular non-signalling proteins (iFGFs; FGF11-14). <ref name="PMID25772309"/>

As illustrated in the image below, FGFRs are comprised of 3 immunoglobulin domains (IgI, IgII, IgIII), with IgIII being the closest to the transmembrane and IgI being the furthest away. Some notable features of this receptor include an acidic box (AD) located in-between IgI and IgII, a heparin-binding domain (HBD) within IgII which is important in signal transduction, and the transmembrane (TM) structure of IgIII which has both kinase and interkinase domains (KD and IKD) within the intracellular space. FGF ligands linked to heparin sulfate proteoglycan (HSPG) bind to both the IgII and IgIII domain of the receptor (with the heparin component specifically binding to IgII) resulting in dimerisation of the receptors and activation of signal transduction pathways through the phosphorylation of tyrosine residues, as discussed in more detail under the subheading signal transduction. <ref><pubmed>16216232</pubmed>[http://www.ncbi.nlm.nih.gov/pubmed/16216232]</ref>

[[File:FGFR receptor subtype.jpeg|thumb|none|300px|Simplistic illustration of the FGFR receptors adapted from review article [http://www.ncbi.nlm.nih.gov/pubmed/16216232 Functions and regulations of fibroblast growth factor signaling during embryonic development]]]

===Subtypes of FGFR===
{| class="pretty table"
|-bgcolor="DDCEF2"
| '''FGFR Subtype''' || '''Function''' || '''Abnormalities'''
|-bgcolor="FAF5FF"
| FGFR1 ||
*Involved in morphogenesis as well as orchestrating the patterning of the mesodermal germ layer at gastrulation<ref><pubmed>16207751</pubmed></ref> 
*Involved in formation of the organ of corti and auditory sensory epithelium <ref><pubmed>12194867</pubmed></ref> 
*Expressed in early limb bud <ref><pubmed>1321062</pubmed></ref> 
*Expressed at epiphyseal growth plate as well as in the perichondrium, prehypertrophic and hypertrophic chondrocytes<ref><pubmed>17169623 </pubmed></ref> 
*Is a negative regulator of bone growth<ref><pubmed>16815385</pubmed></ref> 
||
*Pfeiffer Syndrome (Type 1)
*Kallmann syndrome
*Osteoglophonic dysplasia
*8p11 myeloproliferative syndrome

|-
| FGFR2 ||
*Activated prior to gastrulation with the purpose of repressing cellular movements in the presumptive anterior neural plate and preventing normal retinal progenitor cells from adopting retinal fates<ref><pubmed>14723847</pubmed></ref> 
*Acts as a marker of prechondrogenic condensations<ref><pubmed>9784595</pubmed></ref> 
*Expressed in condensing mesenchyme of the early limb bud<ref><pubmed>1315677</pubmed></ref> 
*Plays a key role in skeleton development as it is expressed in osteoprogenitor cells and differentiating osteoblasts<ref><pubmed>20489451 </pubmed></ref> 
*Is involved in cranial cell replication or differentiation in both humans and mice.<ref><pubmed>15863034 </pubmed></ref> 
||
*Pfeiffer Syndrome (Type 1-3)
*Apert Syndrome
*Crouzon Syndrome
*Beare-Stevenson cutis gryata syndrome<ref><pubmed>17552943 </pubmed></ref> 
|-bgcolor="FAF5FF"
| FGFR3 ||
*Induces complete growth arrest of cells<ref><pubmed>11779141 </pubmed></ref> 
*Is required to promote differentiation of prechondrogenic mesenchymal cells to cartilage-producing chondrocytes <ref><pubmed>8432397 </pubmed></ref> 
*Is expressed in chondrocytes, differentiated initially from the core of the mesenchyme condensation<ref><pubmed>8630492 </pubmed></ref> 
*Is expressed in reserve and proliferating chondrocytes as the epiphyseal growth plate is formed<ref name="PMID 12080084"><pubmed>12080084</pubmed></ref> 
||
*Achondroplasia (can be severe, with developmental delay and acanthuses)
*Thanatophoric Dysplasia
*Hypochondroplasia
|-
| FGFR4 ||
*Involved in proliferation of the blastocyst inner cell mass, differentiation of the presomitic mesoderm and limb bud development<ref name ="PMID 10662638"><pubmed>10662638</pubmed></ref> 
*Regulates cholesterol metabolism, bile acid synthesis and liver mineral homeostasis
*It will provide mitogenic and morphogenic signals to regulate normal limb development<ref name="PMID 12080084"/> 
*Promotes intramembranous ossification and participates in the development of calvarial bone<ref name ="PMID 10662638"/> 
||
*Chondrodysplasia
|-
|}

===Signal Transduction===
 [[File:FGF signalling pathway.jpg|thumb|500px|FGFR Signalling Pathway (Image based upon<ref><pubmed>27458533</pubmed></ref>)]]

The process of signal transduction commences with the binding of a cognate ligand to FGFRs ligand binding site which in turn triggers receptor dimerization. This dimerization of the receptor will cause activation of intrinsic kinase activity<ref><pubmed>1655404</pubmed></ref>. This will activate multiple signal transduction pathways intracellularly including RAS, Mitogen-activated protein kinase (MAPK), p38 MAPKs, Phospholipase-C-Gamma, Crk, Protein Kinase-C and Phospholipase-C-Gamma and Extracellular signal-regulated kinases. Activation of FGFRs induces tyrosine phosphorylation of FRS2 (FGFR stimulated2 Grb2 binding protein) which in turn stimulates the recruitment of GRB2 (Growth factor receptor bound protein-2) and SHP2 ( Src homology 2 phosphatase-2) <ref><pubmed>11021964</pubmed></ref>.
 
 
In turn, this sequence of events promotes sustained activation of RAS, which leads to changes in gene transcription through interactions with DNA. In addition, FGF receptors will also induce the activation of PI3K (phosphatidylinositol-3-Kinase), STAT1 and Src tyrosine kinase, which will contribute to certain FGF-stimulated biological responses <ref><pubmed>1656221</pubmed></ref>.
 
 
With respect to embryonic development, both the PI3K and RAS pathways are essential in order for the normal mesoderm to develop in the embryo. Additionally, receptor-mediated induction of the SHP2-RAS-ERK pathway is a key mechanism through which FGF can activate a variety of biological signalling pathways including cell growth, cellular differentiation as well as morphogenesis <ref><pubmed>9632781</pubmed></ref>.

{| class="wikitable mw-collapsible mw-collapsed"
! YouTube video outlining FGF Signalling Pathway
|-
|<html5media height="400" width="533">https://www.youtube.com/watch?v=DUBelRjjqvc</html5media>
 
This is a YouTube animation which illustrates a simplified version of the FGF Signalling pathway discussed above. This signalling pathway leads to changes to gene expression that, for example, can result in changes in cell growth, division or differentiation.<ref> Oxford University Press (2015, March 9) the FGF Signalling Pathway [Video file]. Retrieved from https://www.youtube.com/watch?v=DUBelRjjqvc </ref>
|}

==Role In Embryonic Development==

===Patterning Of The Embryonic Axis===
In the process of patterning of the embryonic axis, the caudal primordium that is part of the neural plate, contains cells that are rapidly dividing and is able to maintain itself as a growth region (this region is considered to be of "stem cell" status). The expanding populations of dividing cells spread along the neural tube by cell movements of convergence and extension. As cells undergo a process whereby they are driven out of the tube, they change their pattern of movement, which eventually causes a gradual restriction in space<ref><pubmed>8575335</pubmed></ref>. Within this process, it is the misexpression of a dominant negative FGFR construct in the tissue which causes these cells to prematurely leave the stem cell region and to change their movement patterns as if they had aged<ref><pubmed>11389440</pubmed></ref>.

Furthermore, Mathias et al. (2001) suggest that FGFR is required in order to maintain this stem cell status in the caudal neural plate during patterning of the nervous system. In addition, it is possible that FGF serves the purpose of acting as a caudalizing factor for the neural tube because it is capable of prolonging the window of time during which cells are exposed to a caudalizing factor.

In summary, FGF signalling is important in regulating the maturation of developing cells which are gradually being laid down in a caudal direction along the axis of the neural tube.

===Limb Bud Formation===
[[File:LIMB BUD.png|200px|thumb|400px|Mechanisms of FGF signalling during organises; a-c: limb development, d-e: lung development, f-h: induction of the otic placode and differentiation of the otic vesicle<ref name="PMID25772309"/>]]

Limb buds are structures formed early in [[Lecture - Limb Development| limb development]] which are comprised of lateral plate mesoderm (LPM) cells and an overlying surface ectoderm. They are roughly formed around week 4 of embryonic development as a result of interactions between the mesoderm and ectoderm germ layers.

FGF proteins and its interactions with other signalling pathways, are critical for the initiation and proximal-distal growth of limbs from a limb bud structure.<ref><pubmed>9620845</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/9620845]</ref> The following information is accompanied by a YouTube video below and the image on the right, where figures a-c corresponds specifically to limb bud formation<ref name="PMID25772309"/> Prior to limb bud formation, FGF10 is widely expressed in the LPM and is stabilized by the WNT signaling proteins. FGF10 is responsible for stimulating the expression of WNT3 (and downstream transcription factors including SP6 and SP8<ref><pubmed>15358670</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/15358670]</ref>) in the overlying ectoderm, which results in the formation of the Apical Ectodermal Ridge (AER), a specialised thickening of epithelium located towards the proximal end of the bud that is required for growth,<ref name="PMID25772309"/> which subsequently stimulates FGF8. FGF8 is responsible for continued growth of the underlying mesoderm by keeping it in a mitotically active state, and stimulating a positive feedback loop on FGF10 (which in turn stimulates increased FGF8 expression). FGF8 is the known AER-specific FGF to be expressed throughout it, although other FGFs are expressed in the posterior AER (including Fgf4, Fgf9 and Fgf17) and are thought to have supporting roles.<ref><pubmed>11101846</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/11101846]</ref><ref><pubmed>12152071</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/12152071]</ref>
FGFs in the AER signal FGFR1 and FGR2 in distal mesenchyme, activating ETV1 and EWSR1 which function to help to maintain FGF10 expression.<ref><pubmed>25109552</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/25109552]</ref>

Furthermore, the Zone of Polarising Activity (ZPA) is a region located on the posterior side of the limb bud composed of mesenchyme which signals its anterior-posterior growth (for example this region signals the position of the thumb relative to the little finger.) The Fibroblast Growth Factors FGF2<ref><pubmed>7908145</pubmed> [https://www.ncbi.nlm.nih.gov/pubmed/7908145]</ref>, FGF4<ref><pubmed>8001146</pubmed> [https://www.ncbi.nlm.nih.gov/pubmed/8001146]</ref> and FGF8<ref><pubmed> 8598907</pubmed> [https://www.ncbi.nlm.nih.gov/pubmed/8598907]</ref> induce Sonic Hedgehog (SHH) within ZPA region and is critical for its growth along the anterior-posterior axis.

Therefore together these interactions of the FGFs from the AER help to maintain proliferating cells near the distal tip of the limb bud, and are known to be critical in limb bud development, both along the proximal-distal axis and the anterior-posterior axis. It is also important to note that growth along the dorsal-vental axis is dependent on the involvement of growth factors from the Wnt family on the ectodermal layer.

FGF signaling is also involved in lung bud initiation and development, with a similar underlying process.This is supported by the accompanying image on the right, where figures d and e specifically looks at the interplay of FGFs and FGFRs on the lung bud imitation and lung development.<ref name="PMID25772309"/>

{| class="wikitable mw-collapsible mw-collapsed"
! YouTube video outlining limb bud development
|-
|<html5media height="400" width="533">https://www.youtube.com/watch?v=VpbdqGJ9LWk</html5media>
 
YouTube video outlining limb bud development<ref>Itzel García (2012, July 9) Limb development [Video file]. Retrieved from https://www.youtube.com/watch?v=VpbdqGJ9LWk</ref>
|}

===Bone Development===
[[File:FGF and FGFR expression patterns during endochondral and intramembranous bone development.jpeg|thumb|400px|FGF and FGFR expression patterns during endochondral and intramembranous bone development <ref name="PMC4526732"><pubmed>PMC4526732</pubmed>
[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526732/]</ref>]]

Much of what we now understand about the involvement of the FGF signalling pathway in bone development is a result of discovering missense mutations responsible for conditions characterised by abnormal bone structure, including but are not limited to, skeletal dysplasias and craniosysnostosis syndromes (some of which discussed in more detail later under the subheading abnormalities.) The first and questionably the most important mutation discovered affecting skeletal development was a point mutation of the FGFR3 protein, which was found to be responsible for achondroplasia. <ref><pubmed>7913883</pubmed></ref>

FGF signalling is involved in both endochondral and intramembranous [[Lecture - Musculoskeletal Development| bone development]], which are critical in the early stages of embryonic bone formation. As shown in the diagram to the right the presence of FGFR1-3 and FGF2, FGF9, FGF18 are involved in various stages of bone development.

Endochondral bone development (A-D in the figure) is responsible for forming the long bones of the appendicular skeleton, face and spinal column. This involves an intermediate cartilage template (which helps control the growth and patterning of the development of the bony structure.) As shown in the figure provided by a review article<ref name="PMC4526732"/> FGFR signalling is present across different stages of development (ranging from mesenchymal condensation to the establishment of the primary ossification centre. FGFR2 (light blue) expression is prominent in mesenchymal condensation, FGFR1 (white) is uniformly expressed throughout the mesenchyme, and both FGFR3 (red) and FGFR4 (not shown) are not present in distal limb bud mesenchyme and expressed proximally in tissues related to developing muscle. <ref><pubmed>21302260</pubmed></ref> In comparison, intramembranous bone development (G in the figure) is responsible for forming bones of the skull and clavicles, and doesn’t require a cartilage template, it directly forms bone. As shown in the figure provided by a review article<ref name="PMC4526732"/> we primarily see the presence of FGFR1 (white) on mesenchymal cells and both FGFR1 and FGFR2 (dark blue) on osteoprogenitor cells, osteoblasts and osteocytes (in mineralised bone.) Furthermore, this figure also shows FGF and FGFRs involvement in both the Embryonic (E in the figure) and Postnatal Growth Plate (F in the figure) and highlights how they are distributed differently between these two stages of life.<ref name="PMC4526732"/>

For additional information see the recent (2015) review article by Ornitz1 and Pierre [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526732/ ''Fibroblast growth factor signaling in skeletal development and disease'']

===Kidney development===
The metanephric kidney is an organ which arises primarily form two tissues, the nephrogenic cord and the Wolffian duct, which will eventually give rise to the metanephric mesenchyme and the ureteric bud respectively <ref><pubmed>18835385</pubmed></ref>. Around week 5 of gestation in the developing human embryo, the metanephric mesenchyme will release signalling molecules that stimulate the ureteric bud to grow out from the Wolffian duct and invade the metanephric mesenchyme. The stromal mesenchyme that exists between the Wolffian duct and the metanephric mesenchyme restricts the ureteric bud to its proper position and prevents ectopic budding<ref><pubmed>10749566</pubmed></ref>. The metanephric mesenchyme will continue to release signals which will stimulate the ureteric bud to elongate and repeatedly branch, leading to formation of the ureter, collecting duct system and the renal pelvis. Following its contact with the ureteric bud, the metanephric mesenchyme will then divide into a nephrogenic lineage lying adjacent to the bud, and a surrounding renal cortical stromal lineage <ref name="PMID19272374"><pubmed>19272374</pubmed></ref>. Each terminal tip of the ureteric bud induces local areas of nephrogenic mesenchyme in order to differentiate into nephron epithelia, progressing from renal vesicles ,to comma-shaped bodies, to S-shaped bodies, and then to immature nephrons<ref name="PMID19272374"/>. The renal cortical stroma will provide a framework and likely a niche for the other renal lineages and vasculature, and ultimately differentiates into interstitial and other supportive cells within the kidney <ref><pubmed>10594778</pubmed></ref>.

In terms of the development of the metanephric kidney, all FGFRs have been detected in the process of development, however studies using animal models have revealed that it is FGFR1, FGFR2 and FGFR11 which play a key role in renal development <ref><pubmed>10691305</pubmed></ref>. FGFR1 is a receptor which is expressed mostly in the metanephric mesenchyme lineages, these including the early metanephric mesenchyme, the cap mesenchyme and the developing nephrons beginning with vesicles. However, FGFR1 is present at lower levels in the ureteric lineage and in the renal cortical stroma<ref><pubmed>10385628</pubmed></ref>. In contrast, FGFR2 is strongly expressed in the Wolffian duct and the ureteric bud tree as well as the differentiating nephrons. Despite this, FGFR2 is present at lower levels in the early metanephric mesenchyme and stomal mesenchyme adjacent to the Wolffian duct<ref name="PMID1315677"><pubmed>1315677</pubmed></ref>. In addition, FGFR11 is present in renal vesicles <ref name="PMID1315677"/>.

===External Genitalia development===
[[File:External genitalia.jpg|thumb|200px|External genitalia development<ref><pubmed>26081573</pubmed></ref>]]
The genital tubercle (GT) is a structure from which characteristics in the external genitalia in the adult develop. The GT differentiates into a penis in males and a clitoris in females. The process of proximodistal elongation of this GT involves multiple interactions between growth factors and transcription factors <ref><pubmed>3723059</pubmed></ref>. Interactions between epithelium and mesenchyme have an essential role in the regulation of various development processes throughout the embryo. Such signalling controls many aspects of organogenesis, from the initiation of organ development to differentiation <ref><pubmed>8896986</pubmed></ref>.

The FGFR signalling pathway is involved in epithelial to mesenchymal interactions during organogenesis. Studies have revealed that the first morphological sign of GT outgrowth occurs at approximately 10.5 days post coitum, and will continue throughout the perinatal period <ref><pubmed>12004962</pubmed></ref>. Initially within the developing embryo, the external genitalia of the male and female foetuses are morphologically identical and consist of the GT. Several growth factors including FGF proteins have been shown to control external genitalia development in mice <ref><pubmed>10021340</pubmed></ref>. FGF8, FGF10 and FGFR2 expression has been found during GT developing, thus suggesting that a combination of these factors may constitute redundant developmental functions during GT morphogenesis<ref><pubmed>10804187</pubmed></ref>. As the GT elongates, a groove appears on its ventral aspect called the urethral groove. At the distal end, this groove is made up of a solid plate of epithelial cells, the distal urethral epithelium (DUE) that extends into the glans penis. The solid urethral plate canalizes and thus extends the urethral groove distally into the glans. It was found that FGFR2IIIb is expressed in the DUE and urethral plate epithelia of the GT. Deletion of this receptor and FGF10 was shown to cause urethral dysmorphogenesis.

It was also shown that the deletion of FGR2 or FGF10 would result in hypospadias in mice, where when FGFR2 was deleted in the ectoderm leads to severe hypospadias and absence of the ventral prepuce whereas when FGFR2 was deleted in the endoderm, mild hyospadias occurs and maturation of complex urethral epithelium was inhibited<ref><pubmed>26081573 </pubmed></ref>.

===Inner ear development===
[[File:Inner ear development.jpg|500px|thumb|Inner ear development (Image was retrieved from a review article<ref><pubmed>22855724 </pubmed></ref>]]
The inner ear, containing the vestibule and cochlea, is derived from a simple ectodermal thickening called the otic placode. Genetic evidence and expression of data has lead to the suggestion that FGF3 and other fibroblast growth factor types influence early development of the mammalian inner ear, specifically by regulating the formation of the endolymphatic duct <ref><pubmed> 12761848</pubmed></ref>. FGFR-3 is expressed in the cochlear special sensory epithelium, particularly during late embryogenesis and during postnatal life. To reinforce this, further investigations have revealed that FGFR3 absence leads to deafness attributable to disturbances in the differentiation of the cochlear sensory epithelium<ref><pubmed> 8630492</pubmed></ref>. Studies have also revealed that cochlear neuron-derived FGF1 and inner hair cell-derived FGF8 may serve as ligands which bind to FGFR-3 during the late embryonic and postnatal cochlea. In addition, FGF9 mRNA has been localised to the otic vesicle and to the later developing nonsensory epithelium and ganglion of the cochlea<ref><pubmed> 10474167</pubmed></ref>.
 
 
In studies which investigated the dynamic expression patterns of FGF10 and FGFR-2 mRNAs, it was revealed that FGF10 was widely expressed in the undifferentiated otic epithelium however it was subsequently restricted to the presumptive cochlear and vestibular sensory patches. Also, the strong expression of FGF10 mRNAs was found in the otic epithelium-derived neuronal precursors and in the neurons of the cochleovestibular ganglion. Furthermore, te expression of FGF10 mRNA and its colocalization with neurotrophin mRNAs in the ventral patch is indicative that neurons belonging to the inner ear as well as part of the sensory epithelium, have a common origin in this epithelial domain<ref><pubmed> 8071140</pubmed></ref>. In the cranial nerve ganglion, FGF10 mRNA was found within those of the cochlear and vestibular ganglia and not in the surrounding ganglia, which is suggestive that FGF10 relates to the unique colocalization of neurotrophin receptors in the inner ear sensory neurons. Alternative studies have revealed that hindbrain-derived FGF3 has been suggested to regulate patterning of the inner ear, particularly the endolymphatic duct <ref><pubmed>8223243</pubmed></ref>. It was further revealed that FGF3 mRNA is expressed in the ventrolateral region of the otic vesicle at the same stage that it is visible in the hindbrain.

==Animal Models==
===Mouse Models===
Over the past few decades, extensive studies in mice have yielded insights into the roles of various FGF molecules and signalling pathways in embryonic development. In particular, loss-of-function genetic analysis in the mouse has been crucial for understanding FGF function. <ref name ="PMID26666435"><pubmed>26666435</pubmed></ref>

For example, one of the most recent models developed for studying Fgf functions during development, as reported in Genesis in February 2016, is the Fgf3(Δ)-Fgf4(flox)-cis mouse line <ref name="PMID26666435"/>. This model newly allows exploration of redundancy between Fgf3 and Fgf4 genes which are both located on chromosome 7, 18.5 kb apart, by retargeting Fgf3 and Fgf4 in cis, generating an Fgf3 null allele and a conditional Fgf4 allele subject to Cre inactivation. The line showed caudal axis extension defects in Fgf3 mutants to worsen with Fgf4 inactivation, demonstrating redundancy. The model can be applied in the future study redundancy of these genes in a variety of tissues and stages of development.

The following table summarises selected mouse models with germline, conditional or temporarily induced knockout or deficiency for specific FGFs that have been used to certain demonstrate defective aspects of embryological development. Many of these mouse models continue to be used in emerging medical research into the respective pathologies they characterise.
{| class="pretty table"
|-bgcolor="DDCEF2"
| '''Mouse Type''' || '''Phenotype expressed''' || '''Viability in Null Mutant'''
|-bgcolor="FAF5FF"
| Fgf1-, Fgf21- ||
*impaired energy/lipid metabolism, diabetes under high-fat diet<ref><pubmed>22522926</pubmed></ref> <ref><pubmed>23874946</pubmed></ref> 
||
Viable
|-
| Fgf2- ||
*decreased vascular muscle contractility, low blood pressure, thrombocytosis <ref><pubmed>9461194</pubmed></ref> 
*decreased cardiac hypertrophy in ischaemic injury <ref><pubmed>10491406</pubmed></ref> 
*reduced cortical neurogenesis <ref name="PMID 9576942"><pubmed>9576942</pubmed></ref> 
*reduced skin wound healing <ref name="PMID 9576942"/> 
*reduced trabecular bone formation <ref><pubmed>10772653</pubmed></ref>, dwarfism, rickets, osteomalacia <ref><pubmed>25389287</pubmed></ref> 
||
Viable
|-bgcolor="FAF5FF"
| Fgf3- ||
*defective inner ear <ref><pubmed>8223243</pubmed></ref> 
*defective heart <ref name ="PMID21664901"><pubmed>21664901</pubmed></ref> 
||
E15.5 <ref name ="PMID21664901"/> 
|-
| Fgf4- ||
* impaired blastocyst inner cell mass proliferation <ref name="PMID 7809630"><pubmed>7809630</pubmed></ref> 
||
E4-4 <ref name="PMID 7809630"/> 
|-bgcolor="FAF5FF"
| Fgf7- ||
* impaired ureteric bud development, decreased number of nephrons <ref name ="PMID 9876183"><pubmed>9876183</pubmed></ref> 
* prone to seizures <ref><pubmed>20505669</pubmed></ref> 
||
Viable <ref name ="PMID 9876183"/> 
|-
| Fgf8- ||
* failed gastrulation <ref><pubmed>10421635</pubmed></ref> 
* defective kidney development <ref><pubmed>16049111</pubmed></ref> 
* defective limb development <ref><pubmed>11101846</pubmed></ref> 
* defective inner ear <ref><pubmed>15741321</pubmed></ref> 
* defective cerebellum <ref><pubmed>10751172</pubmed></ref> 
* defective heart outflow tract <ref><pubmed>14975726</pubmed></ref> 
||
E7 <ref><pubmed>10421635</pubmed></ref> 
|-bgcolor="FAF5FF"
| Fgf9- ||
* lung hypoplasia <ref><pubmed>16540513</pubmed></ref> 
* male to female sex reversal <ref><pubmed>11290325</pubmed></ref> 
* rhizomelia <ref><pubmed>17544391</pubmed></ref> 
* shortened small intestine <ref>pubmed>18653563</pubmed></ref> 
* cecal agenesis <ref><pubmed>22819677</pubmed></ref> 
* cardiomyopathy <ref name="PMID 15621532"><pubmed>15621532</pubmed></ref> 
* ataxia <ref><pubmed>19232523</pubmed></ref> 
||
P0 <ref><pubmed>11493531</pubmed></ref> 
||
|-
| Fgf10- ||
* lung hypoplasia <ref name="PMID9784490"><pubmed>9784490</pubmed></ref> 
* defective limb development <ref name="PMID9784490"/> 
* defective inner ear formation <ref><pubmed>14623822</pubmed></ref> 
* defective pancreatic development <ref><pubmed>12810586</pubmed></ref> submandibular salivary gland <ref><pubmed>15972105</pubmed></ref> and defective mammary gland <ref><pubmed>16720875</pubmed></ref> 
* defective tracheal cartilage <ref><pubmed>21148187</pubmed></ref> and cleft palate <ref><pubmed>15199404</pubmed></ref> 
* cecal agenesis <ref><pubmed>22819677</pubmed></ref> 
||
P0 <ref name="PMID9784490"/> 
|-bgcolor="FAF5FF"
| Fgf 13- ||
* impaired learning memory and neuronal excitability, neuronal migration defects <ref><pubmed>22726441</pubmed></ref> 
||
Viable
|-
| Fgf14- ||
* impaired learning, memory and neuronal excitability <ref name="PMID 17236779"><pubmed>17236779</pubmed></ref> 
* ataxia <ref><pubmed>12123606</pubmed></ref> and motor weakness <ref name="PMID 17236779"/> 
||
Viable
|-bgcolor="FAF5FF"
| Fgf15- ||
* Heart defects in outflow tract <ref><pubmed>15789410</pubmed></ref> 
* neurogenesis <ref><pubmed>18625063</pubmed></ref> 
* bile acid metabolism <ref><pubmed>16213224</pubmed></ref> 
||
E13.5-P7 <ref><pubmed>15789410</pubmed></ref> 
|-
| Fgf16- ||
* cardiomyopathy <ref name="PMID 15621532"/> 
||
Viable
|-bgcolor="FAF5FF"
| Fgf17- ||
* defective cerebellum <ref><pubmed>10751172</pubmed></ref> and frontal cortex <ref><pubmed>17442747</pubmed></ref> 
||
Viable
|-
| Fgf18- ||
* lung development defects <ref name="PMID 15336546"><pubmed>15336546</pubmed></ref> <ref><pubmed>11927601</pubmed></ref> 
* bone and cartilage development defects <ref><pubmed>26595272</pubmed></ref> 
||
P0 <ref name="PMID 15336546"/> 
|-bgcolor="FAF5FF"
| Fgf20- ||
* kidney agenesis <ref><pubmed>22698282</pubmed></ref> 
* cardiomyopathy <ref name="PMID 15621532"/> 
||
Viable <ref name="PMID 15621532"/> 
|-
| Fgf23- ||
* deafness, defective middle ear development <ref><pubmed>25243481</pubmed></ref> 
* hyperphosphatemia and impaired vitamin D metabolism <ref name="PMID 14966565"><pubmed>14966565</pubmed></ref> 
||
PW12 <ref name="PMID 14966565"/>
|-
|}

===The Importance of FGF10 in Limb and Lung Development in Chicks and Mice===
[[File:Mice model and limb development.gif|thumb|400px|Mice model and limb development<ref name="PMID9784490"/>]]
In vertebrate embryos, initiation of limb buds results from the outward proliferation of the lateral plate mesoderm<ref><pubmed> 9323126</pubmed></ref>. The distal ectoderm surrounding this region is then induced by dividing mesenchymal cells to thicken and form a structure called the apical ectodermal ridge (AER). Molecular interactions that occur between the AER and the underlying mesenchyme are vital in order for proximal-distal patterning to occur. FGF2, 4 and 8 are expressed in the AER of Chicks, and are capable of replacing the AER to induce underlying mesenchyme to maintain its distal outgrowth. The anterior-posterior patterning of each limb bud is regulated by the zone of polarizing activity (ZPA), which is located at the posterior margin of the limb bud mesenchyme<ref name="PMID4826292"><pubmed> 4826292</pubmed></ref>.

Tissue graft experiments have indicated that vertebrate limb bud formation is initiated by factors from mesoderm within the limb field<ref name="PMID4826292"/>. Implantation of beds soaked in FGFs or FGF-expressing cells is capable of inducing formation of ectopic limbs within chick embryos. FGF 1, 2, 4, 8 and 10 were shown to exhbit limb-inducing activity<ref><pubmed> 7889567</pubmed></ref>. However, only FGF8 and FGF10 will express demonstrate the correct temporal and spatial expression that could guide the initiation of the limb bud. FGF8 in chick embryos is expressed in the intermediate mesoderm at presumptive limb regions before limb bud initiation. This is compared to FGF10, which is only expressed in the lateral plate mesoderm within the limb field prior to limb bud initiation, and the expression persists in the mesenchyme under AER after initial limb bud formation<ref><pubmed> 8674413</pubmed></ref>.

Evidence also suggests that FGF10 may also affect development of the vertebrate lung. In mice, the process of lung morphogenesis begins with ventral extension of the laryngotracheal groove from the primitive gut endoderm approximately at E9.5. After this stage, the tracheal primordium will bifurcate to produce left and right principal bronchi, around which the lung buds differentiate. Further branching of these bronchi result in the development of bronchioles and alveoli that form mature lung parenchyma. A recent study suggests that an FGF-mediated signal plays a major role in lung development. A splice variant of FGFR2 is highly expressed in respiratory epithelium during early branching morphogenesis in the epithelium of the respiratory tract during early branching morphogenesis<ref><pubmed> 15632068</pubmed></ref>.In further investigations, when FGF10 was absent in the developing embryos of mice, there was complete absence of budding limbs at E9.5 whilst all other external structures remained. Thus these results suggest that FGF10 is necessary for limb bud initiation<ref name= "PMID9784490"/>.
 

==Abnormalities==
As discussed above, the FGF signalling pathway is critical for regulating many early embryonic developmental processes, and is critical for normal organ, vascular and skeletal development. Consequently, abnormalities in genes coding for the proteins within this signalling pathway (including signalling proteins, non-signalling proteins, and receptors) can result in many visible structural abnormalities such as short statue and face deformations. Not to mention that a large majority of these conditions, if not all, influence an individual’s quality of life, and in some cases increase risk of fatality. Some of these FGF abnormalities are outlined in more detail below, including Achondroplasia, Pfeiffer and Apert Syndrome which particularly emphasise the significance of FGF signalling in early skeletal development.

===Achondroplasia===
Achondroplasia is the most common form of skeletal dysplasia, and is often characterised by shortened proximal limbs, a curved spine, a large prominent forehead and a fattened nasal bridge. This condition is inherited genetically as an autosomal dominant trait, although a large proportion of cases are sporadic. <ref><pubmed>7913883</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/7913883]</ref> This condition results in reduced inhibition of endochondral ossification, which is one of the main way in which bone tissue is created during embryonic development (the other being intramembranous ossification.) Endochondral ossification is essential during development for both the formation and growth of long bones as well as healing fractures. For the majority of affected individuals, it is a result of a missense mutation in FGFR3, specifically due to a substitution of arginine for glycine (G380R).<ref><pubmed>12816345</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/12816345]</ref> As originally postulated by Bonaventure et al. (1996) this introduction of a hydrophilic residue in a hydrophobic receptor domain results in a disruption of alpha-helical structure of the transmembrane portion of the protein and consequently interferes with the signal transduction pathway of which it is involved in. <ref><pubmed>8723101</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/8723101]</ref>

There are other mutations in FGFR3 which are responsible for different skeletal developmental conditions, including a more severe (usually fatal) form of skeletal dysplasia, Thanatophoric Dysplasia, which is due to two different mutations, K650E and R248C in FGFR3 (type 1 and type 2 respectively) and a milder form, hypochondroplasia, which is due to the mutations, N540K or K650N in FGFR3. Recent studies have also shown expression of an fgf4 retrogene to be associated with achondroplasia in domestic dogs. <ref><pubmed>19608863 </pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/19608863]</ref>

===Pfeiffer Syndrome===
Pfeiffer syndrome is characterised by craniosynostosis, meaning that is it a condition where the cranial fibrous sutures prematurely fuse (ossify) resulting in a reduced space for the growing brain. Subsequently, abnormal growth of the skull, in an attempt to increase the space available for the brain and reduce cranial pressure, results in the development of abnormal facial features including, but not limited to, proptosis (abnormal placement of the eye), hypertelorism (abnormal increase in distance between the eyes), maxillary deficiency, and a beaked nose. Other notable features include those of the hands, broad thumbs and the feet, medially deviated broad great toes.
<ref><pubmed>9300656</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/9300656]</ref><ref name= "PMID25679016"><pubmed>25679016</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/25679016]</ref> This condition is inherited genetically as an autosomal dominant trait. There are 3 types of Pfeiffer syndrome. Type 1 is a result of either a gain of function P252R mutation of FGFR1 (5%), which increases the receptor’s ligand binding affinity resulting in over-activation of the receptor, or sequence variants of FGFR2 gene (95%.)<ref name= "PMID25679016"/> Type 2 and 3 are similar, both appear more severe and generally have a worse prognosis compared to Type 1, and are a result of mutations of the FGFR2 gene.
<ref><pubmed>8434615</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/8434615]</ref><ref><pubmed>10394936</pubmed>[https://www.ncbi.nlm.nih.gov/pubmed/10394936]</ref>

{| class="wikitable mw-collapsible mw-collapsed"
! YouTube video outlining Pfeiffer Sydrome
|-
|<html5media height="400" width="533">https://www.youtube.com/watch?v=UKYcDm2QHtU</html5media>
 
YouTube video outlining Pfeiffer Sydrome<ref>wyscrvr (2011, March 23) Pfeiffer Syndrome [Video file]. Retrieved from https://www.youtube.com/watch?v=UKYcDm2QHtU</ref>
|}

===Apert Syndrome===
[[File:Syndactyly.jpg|thumb|200px| Syndactyly of the fingers]]
Apert syndrome is characterised by craniosynostosis, as well as turribrachycephaly (high, prominent forehead), midface hypoplasia (incomplete/underdevelopment) and syndactyly (cutaneous and bony fusion) of the fingers and toes. This condition is inherited genetically as an autosomal dominant trait. It is a result of a gain-of-function mutation of FGFR2, specifically at S252W or P253R region, which is responsible for increased receptor affinity for the binding ligand and subsequently result in excessive activation of the receptor. <ref><pubmed>26220993</pubmed></ref><ref name= "PMID25679016"/> It is currently thought that the P253R mutation will increase the affinity of FGFR2 to all FGFs, whereas the S252W mutation on the other hand will increase the affinity of FGFR2 only to a selective subset of FGFs. <ref><pubmed>11390973</pubmed></ref> The genotype of the mutation is thought to explain clinical variability in the presentation of the condition in patients. <ref name= "PMID25679016"/>

==Quiz: How much do you really know about FGF? Take the quiz and find out!==

<quiz display=simple>

{ Which of the following statements regarding FGFR3 is true?.
|type="()"}
- Mutation in the receptor causes Pfeiffer Syndrome
+ Induces complete growth arrest of cells
- Prevents chondrocytes from developing
- Associated with Kallmann syndrome
|| FGFR3 has many roles ranging from its role in promoting differentiation of prechondrogenic mesenchymal cells to cartilage thus producing chondrocytes to inducing complete growth arrest of cells. This will mean that cell growth will come to a complete hault. Thus option B is correct.

{ Which of the following describes FGFR as a receptor type
|type="()"}
- G-protein coupled receptor
- Tyrosine kinase receptor
- Electrically coupled receptor
+ None of the above
|| FGFR are a tyrosine kinase receptor type. Thus meaning, the binding of an extracellular ligand will induce receptor dimerization. This process will allow a tyrosine in the cytoplasmic portion of the receptor to be trans-phosphorylated by its adjacent receptor, which in turn induces a signal through the plasma membrane. Thus option B is the correct.

{ Which of the following is true
|type="()"}
- FGFR attaches at the outer surface of the lipid bilayer
- FGFR attaches on inner surface of lipid bilayer
+ FGFR cross the membrane and is thus transmembrane
- Options A and B
|| Upon observing the illustration of FGFR at the beginning of this page, it is clear that the receptor itself will traverse the lipid bilayer of the cell. Thus option C is correct.

{ How many FGFRs have been discussed in this page?

|type="()"}
- 1
- 2
- 3
+ 4
|| Observing the table of the different types of FGFRs that have been discovered it is clear that there are four types of FGFRs. Thus, option D is the correct answer.

{ Which of the following molecules will directly bind to the DNA in the final stages of the signal transduction pathway?

|type="()"}

+ATF2 and Elk1
-FAS2 and Raf1
-PLD and Rac1
-PKC and IP3

|| Signalling molecules which bind the DNA molecule are capable of altering gene expression within the cell. In the process of FGFR signalling, the two molecules which do this are ATF2 and Elk1, thus the correct answer is A.

{Which statement is correct?
-The use of an anti-FGFR3 antibody for treatment in skeletal-related disorders has no risk of side-effects or toxicity
+ Genetic inactivation of ERK1 and ERK2 in chondrocytes can promote enlargement of the spinal canal
- Genetic activation of ERK1 only can cause apoptosis of cells within the spinal canal
-ERK1 has been proven to inhibit the formation of chondrocytes in the process of bone growth

|| In a study, it was revealed that when ERK1 and ERK2 in chondrocytes are inactivated, this can promote the enlargement of the spinal canal as well as promote the process by which bone develops. Thus the correct answer is B

{ Regarding lung small cell cancer, one which is very aggressive, abnormalities in FGF signalling have been demonstrated in the pathogenesis of this disease. In the process:
-FGF2 is underexpressed
-FGFR1 is reduced significantly
+FGF2 is over expressed
-FGF9 is over expressed

||Lung small cell cancer is a type of cancer that has the ability to metastasise at very early stages which is why it is considered to be deadly. In studies discussed in the above table which links FGF abnormalities to disease, it has been revealed that over expression of FGF2 is an event that occurs in small cell carcinoma. Thus option C is correct.
</quiz>

===Additional Information Regarding Abnormalities in FGFR Signalling===
The abnormalities regarding the FGFR signalling pathways that have been discussed above are widely researched and reported on. However, there are many more conditions resulting from mutations in the FGFR signalling pathway and always ongoing research into these conditions in which it causes. For more information regarding the conditions mentioned above, and in general abnormalities of FGFR signalling, links to OMIM have been provided below.

{{About OMIM}}
Conditions Mentioned Above:
* [http://omim.org/entry/100800 Achondroplasia]
* [http://omim.org/entry/101600 Pfeiffer Syndrome]
* [http://omim.org/entry/101200 Apert Syndrome]

Fibroblast Growth Factor Receptor Subtypes:
* [http://www.omim.org/entry/136350 Fibroblast Growth Factor Receptor 1]
* [http://www.omim.org/entry/176943 Fibroblast Growth Factor Receptor 2]
* [http://www.omim.org/entry/134934 Fibroblast Growth Factor Receptor 3]
* [http://www.omim.org/entry/134935 Fibroblast Growth Factor Receptor 4]

===FGF and FGFR Abnormalities in Cancer===

Deregulation of FGF signaling pathways have been implicated in many types of human and animal cancers <ref name= "PMID25772309"/>. This deregulation can be heritable or acquired during development or postnatally.

These abnormalities in signalling may arise from mutations in genes for FGF ligands, receptors, or downstream signaling pathways, as well as modified protein or gene expression of ligands or receptors at the transcriptional level or via gene amplification. Mechanisms of FGF ligand activation include aberrant expression and gene amplification leading to ligand overexpression, resulting in excessive FGF signaling. Secondary mutations that increase diffusion of FGFs through tissue or increase affinity for FGFRs may also contribute. FGFRs can also be activated by mutations, gene amplification leading to receptor overexpression, or by translocations resulting in activating fusions with adjacent genes. Activation of FGFRs by somatic acquisition of missense mutations is another common tumorigenic mechanism. Each of these mechanisms ultimately results in cancer initiation or progression.

Recent advancements in understanding these pathogenic mechanisms in FGFs and FGFRs has led to therapeutic approaches for a variety of cancers. <ref><pubmed>23696246</pubmed></ref>

The following table describes the types of FGF and FGFR genetic mutations associated with numerous of the most common cancers in humans and their prevalence.

{| class="pretty table"
|-bgcolor="DDCEF2"
| '''Carcinoma Type''' || '''FGF/FGFRs Associated''' || '''% Affected (if known)'''
|-bgcolor="FAF5FF"
| Bladder ||
*over expression of FGF2 <ref><pubmed>20299037</pubmed></ref>
*amplification, translocation and missense mutation in FGFR3 <ref><pubmed>17255960</pubmed></ref> <ref><pubmed>23175443</pubmed></ref>
||
*FGFR3 was amplified in 3% <ref><pubmed>24898159</pubmed></ref>
*missense mutations in FGFR3 have been observed in 35% <ref><pubmed>10471491</pubmed></ref>
|-
| Breast ||
*amplification of FGF3 and FGF4, over expression of FGF8 <ref><pubmed>11953856</pubmed></ref> <ref><pubmed>10023681</pubmed></ref> and FGF10 <ref><pubmed>15208658</pubmed></ref>
*amplification of FGFR1 and FGFR2 <ref name = "PMID 23270564"><pubmed>23270564</pubmed></ref>, over expression and missense mutation in FGFR3 <ref><pubmed>11329138</pubmed></ref>, missense mutation in FGFR4 <ref><pubmed>16822847</pubmed></ref>
||
*FGFR1 amplification identified in 20% lobular breast cancer <ref name = "PMID 23270564"/>
*FGFR4 amplification found in 10% primary breast tumors <ref><pubmed>8099571</pubmed></ref>
|-bgcolor="FAF5FF"
| Colorectal ||
*amplification and missense mutation in FGFR2 and FGFR3 <ref><pubmed>11325814</pubmed></ref>
*missense mutation in FGFR4 <ref name ="PMID 20844967"><pubmed>20844967</pubmed></ref>
||
*FGFR4 mutation present in 57% of patients <ref name ="PMID 20844967"/>
|-
| Glioblastoma ||
* over expression of FGF5 <ref><pubmed>18362893</pubmed></ref>
* over expression and translocation of FGFR1, translocation of FGFR3 <ref><pubmed>22837387</pubmed></ref>
||
* 3.1% exhibit FGFR1 or FGFR3 mutation
|-bgcolor="FAF5FF"
| Hepatocellular ||
* over expression of FGF2 <ref><pubmed>15836707</pubmed></ref>, FGF8 <ref><pubmed>21319186</pubmed></ref>, FGF15/19 <ref><pubmed>22309595</pubmed></ref>, FGF17, FGF18 <ref><pubmed>21319186</pubmed></ref>
* over expression of FGFR4 <ref><pubmed>25031272</pubmed></ref>
|-
| Leukemia & Lymphoma ||
* translocation of FGFR1 <ref><pubmed>9425908</pubmed></ref>
||
|-bgcolor="FAF5FF"
|Lung Adenocarcenoma ||
*over expression of FGF7 <ref><pubmed>15307144</pubmed></ref> and FGF9 <ref><pubmed>23867472</pubmed></ref> <ref><pubmed>25413587</pubmed></ref>
*FGFR1 amplification <ref name = "PMID21666749"><pubmed>21666749</pubmed></ref>
||
*FGFR1 amplification identified in 3% <ref name = "PMID21666749"/>
|-
|Lung Squamous Cell ||
*amplification of FGFR1 <ref><pubmed>24302556</pubmed></ref>
*translocation of FGFR3 <ref><pubmed>23661334</pubmed></ref>
||
*FGFR1 amplification identified in 21-28% cases <ref><pubmed>21160078</pubmed></ref> <ref><pubmed>24302556</pubmed></ref>
|-bgcolor="FAF5FF"
|Lung Small Cell||
* over expression of FGF2 <ref><pubmed>11165400</pubmed></ref>
* amplification of FGFR1 <ref name= "PMID 24294370"><pubmed>24294370</pubmed></ref>
||
*43.7% exhibit FGFR1 amplification, with worse prognostic outcomes <ref name= "PMID 24294370"/>
|-
| Lung Non-Small Cell||
*over expression FGF9 <ref name="PMID 24239165"><pubmed>24239165</pubmed></ref>
||
*10%, with 3-fold increase in likelihood of post-operative occurrence<ref name="PMID 24239165"/>
|-bgcolor="FAF5FF"
| Melanoma <ref><pubmed>8311116</pubmed></ref> ||
*over expression of FGF2
*missense mutation and amplification of FGFR1
||
|-
|Ovarian||
*amplification of FGF1 <ref><pubmed>17538174</pubmed></ref>, overexpression FGF16 <ref><pubmed>24253043</pubmed></ref>
*amplification of FGFR1, over expression of FGFR4 <ref><pubmed>16822847</pubmed></ref> <ref><pubmed>23344261</pubmed></ref>
||
|-bgcolor="FAF5FF"
|Pancreatic ||
* amplification of FGFR1 <ref><pubmed>12105858</pubmed></ref>
||
* 2.6-4% <ref><pubmed>23808822</pubmed></ref>
|-
|Prostate||
*over expression of FGF2 <ref><pubmed>23243019</pubmed></ref>, FGF6 <ref><pubmed>10945637</pubmed></ref>, FGF8 <ref><pubmed>12778074</pubmed></ref>, FGF10 <ref><pubmed>18068633</pubmed></ref>, FGF15/19 <ref><pubmed>23440425</pubmed></ref>, FGF17 <ref><pubmed>15129425</pubmed></ref>, polymorphism in FGF23 <ref><pubmed>24053368</pubmed></ref>
*amplification of FGFR1 and FGFR2 <ref name="PMID14614009"><pubmed>14614009</pubmed></ref>
||
*FGFR1 or FGFR2 was amplified in 47% of hormone resistant prostate cancers <ref name="PMID14614009"/>
|-
|}

==New and emerging research surrounding FGFRs==
===Promising therapeutic methods to alleviate the skeletal phenotypes resulting from dysfunction FGFs/FGFRs===
[[File:Bone signalling pathway1.gif|thumb|400px|Signals regulating bone growth]]
A variety of studies have been conducted in order to investigate methods that will alleviate the skeletal phenotypes caused by dysfunctional FGFs/FGFRs signalling. In gain of function mutations, the major strategy of treatment is to reduce their excessive activities, subsequently alleviating the impaired cell functions, whilst in contrast, loss of function mutations or deficiency are treated by supplementation of related factors <ref><pubmed>15310757</pubmed></ref>.
 
 
In order to prevent excessive intracellular signalling and to alleviate the symptoms of FGFs and FGFR-related genetic disorders, a variety of molecules targeting FGFRs or their tyrosine kinase were used. A soluble form of the Apert mutant, FGFR2, which lacked the transmembrane and cytoplasmic domains, will compete for ligand binding with FGFRs, thus enhancing the process of osteoblastic differentiation of cells in the osteosarcoma cell line transfected with the Apert mutant. Recently, it was found that FGFR2 may partially prevent craniosynostosis in the Apert mouse model <ref><pubmed>17694057</pubmed></ref>. There has also been an increase in the number of studies related to FGFR3-related skeleton disorders. A31, which is a tyrosine kinase inhibitor, is a capable of restoring normal expression of cell cycle regulators and allow pre-hypertonic chondrocytes to properly differentiate into hypertonic chondrocytes in cultured femurs from achondroplasia (ACH) mice<ref><pubmed>22072392</pubmed></ref>. In addition, further research has been able to develop a recombinant protein therapeutic approach which uses a soluble form of FGFR3, as a decoy receptor, in order to rescue the phenotype of ACH transgenic mice with no toxicity<ref><pubmed>24048522</pubmed></ref>. Another approach to target FGFR3 is to use an anti-FGFR3 antibody, however the antibody may carry a risk of an antibody-dependent cell cytotoxic reaction, which prevents its use in ACH.
 
 
Studies have also demonstrated that ERK, a molecule downstream of the FGFR signalling pathway, is responsible for retarded growth of long bones and premature fusion of the synchondroses caused by abnormal FGFR3 expression<ref name= "PMID9069288"><pubmed> 9069288</pubmed></ref>. Genetic inactivation of ERK1 and ERK2 in chondrocytes can promote the enlargement of the spinal canal and promote bone growth. From another study it was found that inhibition of ERK signalling may enlarge the narrowing of the spinal canal, thus alleviating neurological complications of ACH. <ref name= "PMID9069288"/>.

 
 
 

===Emerging Research Into The Role Of FGF In The Development Of The Growth Plate===
https://www.ncbi.nlm.nih.gov/pubmed/25114206
 
===Autoregulatory loop of induction between FGF10 and FGF8 ===
 
 

FGFR2 is a membrane spanning receptor that acts as a receptor for members of the fibroblast growth factor family. By mutating the FGFR2 in mice, a number of novel findings were determined regarding the importance of this receptor <ref><pubmed>9435295</pubmed></ref>. None of the embryos with mutated FGFR2’s survived due to the resulting developmental deficits from a dysfunctional FGFR2. Furthermore, induction of FGF8 is blocked in the limb ectoderm and the expression of FGF10 in the underlying mesoderm is reduced. This highlights the importance of the FGFR2 receptor as well as indicating its involvement in a signalling loop between FGF8 and FGF10. Due to the functions of FGF8 and FGF10, it has been postulated that interaction between these two FGF members is imperative for limb bud formation, in the context of the epithelial – mesenchymal interaction.

Whilst the role of FGFR2 has been described in the context of FGF8 and FGF10, it is important to acknowledge that there are many other pathways that use these fibroblast growth factors and interrupting these will result in similarly disastrous issues. For example, by inhibiting B – catenin activity, limbs will become truncated, indicating FGF-10 being affected and FGF8 expression in the ectoderm was severely down regulated<ref><pubmed>11290326</pubmed></ref>. This shows how the signalling loop between FGF8 and FGF10 can be affected in many different ways and in this instance, by altering the amount of B – Catenin available to the embryo.

== Further Information Regarding FGFR Signalling and Embryology==

{| class="wikitable mw-collapsible mw-collapsed"
! Recent Papers From PubMed
|-
|{{Most_Recent_Refs}}
Search term: ''FGF Signalling In Organogenesis''

<pubmed limit=5>FGF Signalling In Organogenesis</pubmed>
|}
{| class="wikitable mw-collapsible mw-collapsed"

 
 
 

 

==Glossary==
Glossary definitions are sourced from lectures presented in the UNSW embryology course ANAT2341 (in addition to the glossary provided online in the course, which is linked to at the bottom of these selected terms which are related to this page.)
{| class="pretty table"
|-bgcolor="DDCEF2"
|'''Term'''
|'''Definition'''
|-bgcolor="FAF5FF"
|'''Apical Ectodermal Ridge (AER)'''
|Is a term used to describe the specialised thickening of the epithelium located towards the tip of the limb bud, it is formed by Wnt signalling and secrets FGFs which stimulates proliferation and outgrowth. It acts as a signalling centre ensuring appropriate limb development, including the patterning of the proximal-distal axis of the limb. For more information see [[Musculoskeletal System - Limb Development| Limb Development]]
|-
|'''Autosomal Dominant Inheritance'''
| A term used to describe the pattern of inheritance whereby one copy of a gene containing a mutation is sufficient to manifest into the disease. For more information see [[Abnormal_Development_-_Genetic#Genetic_Inheritance |Genetic Inheritance]]
|-bgcolor="FAF5FF"
|'''Craniosysnostosis Syndromes'''
| Are conditions where the cranial fibrous sutures prematurely fuse (ossify) resulting in a reduced space for the growing brain. The skull compensates for this fusion by growing parallel to the suture, meaning that the skull is abnormally shaped.
|-
|'''Ectoderm'''
|One of the initial germ cell layers formed during gastrulation (the others being endoderm and mesoderm). It is the outmost layer and is responsible for the formation of the nervous system and the entire epithelial layer of skin covering the embryo. For more information see [[Ectoderm | Ectoderm]]
|-bgcolor="FAF5FF"
|'''Endoderm'''
|One of the initial germ cell layers formed during gastrulation (the others being ectoderm and mesoderm). It is the innermost layer and is responsible for the formation epithelial lining of the gastrointestinal and respiratory tract, as well as contributions to the accessory organs of the GIT. For more information see [[Endoderm | Endoderm]]
|-
|'''Endochondral Ossification'''
| Is one of the two processes that are critical in the early stages of embryonic bone formation. (The other being intramembranous ossification, see below.) This process involves an intermediate cartilage template and is essential for the formation and growth of long bones of the appendicular skeleton, face and spinal column. For more information see [[Lecture - Musculoskeletal Development| Bone Development]]
|-bgcolor="FAF5FF"
|'''Fibroblast Growth Factors (FGFs)'''
| Are a family of 22 proteins, 18 of which are secreted signalling proteins (FGF1-10, and FGF16-23) and the other 4 are intracellular non-signalling proteins (iFGFs; FGF11-14)
|-
|'''Fibroblast Growth Factor Receptors (FGFRs)'''
| Are a family of 4 tyrosine kinase receptors (FGFR1-4) that interact with the signalling FGF proteins
|-bgcolor="FAF5FF"
|'''Gastrulation'''
| Is the process whereby the trilaminar embryo formed containing the three germ layers (endoderm, ectoderm and mesoderm). For more information see [[Gastrulation| Gastrulation]]
|-
|'''Germ Layers'''
| Refers to the three layers: (endoderm, ectoderm, mesoderm) which are primary cell layers from early in embryogenesis, which give rise to all tissues and organs
|-bgcolor="FAF5FF"
|'''Intramembranous Ossification'''
| It is one of the two processes that are critical in the early stages of embryonic bone formation. (The other being endochondral ossification, see above.) It directly forms bone, it doesn’t require a cartilage template like endochondral ossification. It is responsible for the formation of bones of the skull and clavicles. For more information see [[Lecture - Musculoskeletal Development| Bone Development]]
|-
|'''Limb Bud'''
| The initial embryonic structures responsible for the formation of the paired upper and lower limbs. For more information see [[Musculoskeletal System - Limb Development|Limb Development]]
|-bgcolor="FAF5FF"
|'''Lung Bud'''
| The initial embryonic structures responsible for the formation of the lungs. For more information see [[Lecture - Respiratory Development | Respiratory Development]]
|-
|'''Mesenchymal Tissue'''
|(also Mesenchyme) is a term used to describe cellular organisation of undifferentiated embryonic connective tissue, Its contributions include both mesoderm and neural crest, which are responsible for forming most of the adult connective tissue
|-bgcolor="FAF5FF"
|'''Mesoderm'''
| One of the initial germ cell layers formed during gastrulation (the others being ectoderm and endoderm). It is the middle layer and is responsible for the formation of all the connective tissue of the body (with the exception of the head region which has additional contributions from the neural crest.) For more information see [[Mesoderm | Mesoderm]]
|-
|'''Missense Mutations'''
| A point mutation, replacement of a single nucleotide, which results in a different codon (coding for a different amino acid, this is considered to be a type of non-synonymous substitution)
|-bgcolor="FAF5FF"
|'''Morphogenesis'''
|Is a term used to describe the process of development involving a change in form (shape)/size of either cells/tissues
|-
|'''Phenotype'''
|Is a term used to describe the observable characteristics of an organism and is related to the expressed genotype
|-bgcolor="FAF5FF"
|'''RAS'''
| A family of related proteins which is expressed in all animal cell lineages and organs.
|-
|'''Sensory Placode'''
|Is a thickening of surface ectoderm present (paired) in the head region of the early embryo which contribute to a different component of each sensory system (including the otic placode, optic placode, olfactory placode.) For more information see [[Lecture - Sensory Development | Sensory Development]]
|-bgcolor="FAF5FF"
|'''Skeletal Dysplasia'''
| A general term that relates to disorders affecting normal bone development
|-
|}

''Below are links to a more extensive glossary if additional definitions are needed''

[[A]] | [[B]] | [[C]] | [[D]] | [[E]] | [[F]] | [[G]] | [[H]] | [[I]] | [[J]] | [[K]] | [[L]] | [[M]] | [[N]] | [[O]] | [[P]] | [[Q]] | [[R]] | [[S]] | [[T]] | [[U]] | [[V]] | [[W]] | [[X]] | [[Y]] | [[Z]]

''Some external links were included throughout this page.''
{{External Links}}

==References==

<references/>

Talk:2016 Group Project 3

2016-10-22T04:20:15Z

Z5015337: /* Comments by Group 3 */

{{ANAT2341Project2016discussionheader}}

==Peer Review==

===Group 3 peer assessment===
On browsing through your page for the first time, I was extremely impressed with the organisation and the headings and subheadings. It made it extremely easy to comprehend the well researched information provided in an efficient manner. I thought the incorporation of an overview of the pathway was really good but could be included in the introduction maybe? The hand drawn diagram was very informative and showed good understanding of the topic. The quiz at the end is a different and useful element to add to the page as well and helps to improve our understanding on the topic. Incorporating tables and diagrams is always a great idea so well done on that! The referencing has also been done in an organised and appropriate format. The flow of the page is great as well.

Some points of improvement include making sure all the abbreviations have been written in their full form when used for the first time on the page. For example, EWSR1. I think another thing that can be included is a small description on the important molecules of the pathway.
For the quiz a link could be attached to the ‘submit’ option taking you to a page with the correct answers and explanations as well.
The abnormalities could maybe include a sentence on the current treatment procedures for the same. Or this could be a separate heading all together. This could be included to get a wholesome idea of the abnormality from pathogenesis to treatment.

Overall, I think this is an amazing start to the project and you guys have done a great job covering all aspects of the assessment criteria. I’m sure this is going to be an awesome page!

===Group 3 Peer Review===
Good Job Group 3! Very Well organised page with amazing contents. The signalling pathway is well illustrated with your hand drawing. A lot of articles were reviewed although some more citations may be required for some sentences on the page. The history section is really good making the page very interesting. Developmental effects and abnormalities are also described. Some sections need to be filled in. Seems that you guys are trying to make a few quiz questions in the end, that's a really good idea. Quizzes can definitely improve our understanding about the signalling pathway.

About the introduction part, it may be better if you can combine the introduction, history and overview together. Those three sections posses similar function--provide background information and attract the reader, therefore, i think it would be good to put them together, at least, make history and overview two subsections of introduction. Moreover, the format of the table for FGFR subtypes can be adjusted. Thirdly, I understand that some theories are well studied or well proved, however, it would be better if you can find more recent articles.

Overall, this web page is really good. It is well structured and only some sections need to be completed. I really recommend using of more recent articles because our understanding about the pathway will improve over time. Maybe read through some related articles, they will usually validate the previous results first before they start their own experiments.

===Group 3 Peer Review===
At first glance, your page looks well structured with lots of information present so well done! Your introduction is concise but effective and it provides a good outline of the topic. It’s also good that you’ve started to explain the history - I think the timeline will be really helpful once it’s finished. All your referencing looks to be correct and most of the abbreviations are all defined. The table of subtypes of FGFR is a great way to present this info briefly and clearly, and I really like that you’ve also listed the associated abnormalities. Also, your hand-drawn image is a great effort but it would be better to clearly explain all the abbreviations (at least on the actual image summary page, or maybe in the glossary) since it’s not all defined in the text. You guys have done a really great job so far in explaining the different roles in embryonic development and it’s especially good that you’ve included descriptions of primary research. And your image for bone development is a really helpful addition to your info.

Obviously your group still has some research and info to fill out in your sections but you’ve done really well so far. For your abnormalities section, I think it would be good if you can find some related pictures to include. In general I think you should add more content and explain your sections in some more detail - particularly the overview of the pathway and the signal transduction section. At the moment it’s more of a description/listing of the components and factors, rather than a full explanation of how they interact and the responses they induce. So as long as you guys get fill out your content a bit more and make sure to finish off your quiz, history, animal models, and new/current research sections then I think you will have a great page by the end.

===Group 3 Peer Review===

'''Positive Factors'''

Overall Group 3 has made a really comprehensive effort at addressing the assessment criteria so far. The flow and amount of information covered by this Group is really impressive, showing that they have begun to cover criteria 1, 2, 3 and 5. The range of tools used to convey information (tables, diagrams, the quiz) make this Group’s page a lot more engaging, particularly for a student audience (covering criteria 4). The use of in-text links to wiki pages describing certain terms is also a positive aspect, which lets the readers gain a better understanding of relevant areas of embryology (covering criteria 6).

'''Points for Improvement'''

Some improvements that could be made to this page include: the use of in-text links directly to the glossary to better aid students’ understanding of specific terms used throughout the explanations (this would better address criteria 4); using more succinct headings in some areas such as that under the ‘New and Emerging Research Into FGF’ section; and also a more extensive timeline could be used.

'''Overall'''

In conclusion, Group 3 have a lot of strengths in their work so far, particularly the volume of information they have provided that is formatted in an engaging and logical way. Only a few improvements are necessary for this Group’s project as it seems they have already begun to address most of the assessment criteria.

===Group 3===

You guys have made a good start on your project! I particularly liked how the headings were subdivided appropriately into smaller subheadings as it effectively broke down the FGFR pathway and made the page easy to navigate. Though you have included a short and succinct introduction, I think it should address all the sections being discussed to give the reader a better overview of your project. In addition, the use of a table to explore the timeline of research of the FGF pathway was an excellent idea but I think the text above the table could be incorporated into the table itself and a more extensive timeline could be provided.

Though it was good that you provided a brief overview of the FGFR pathway, you’ve only discussed the components of the pathway rather than the pathway itself. Furthermore, when discussing signal transduction, I think you should be more specific when explaining the process, for example when you mentioned ‘which leads to changes in gene transcription through interactions with DNA’, it causes changes in transcription in which genes and through interactions with which DNA? In saying this, it was wonderful to see the inclusion of a hand-drawn diagram which represents not only your understanding of the pathway but also aids readers understanding of the FGFR pathway.

A good overview has been provided to explain the role of FGFs in embryonic development. The only suggestion I can make is to provide explanations or full names of the abbreviations to aid understanding of the concepts explored. For example, what is ETV1 and EWSR1? By explaining what these abbreviations are the reader will gain better understanding on how they function to help maintain FGF10 expression. In terms of the section on abnormalities, a succinct and coherent introduction was provided. There was a good description of the morphological changes produced by these mutations along with the cause of these abnormalities. There isn’t much I would change in this section except for maybe explaining FGFR2 mutation.

Overall, you guys have done a fantastic job! I thought the inclusion of a quiz was particularly innovative as it makes your project interactive and thus, aids the learning process. Everything was well cited and referenced and it was wonderful to see the use of an original diagram. It was also good to see all groups members contributing to the discussion page which indicates effective communication within the team.

===Group 3 Critical Assessment===
A great introduction to the topic, allowing the reader to slowly transition into the more in-depth points! I particularly like how you have broken down the different constituents of the pathway such as the receptors and protein subtypes and provided a succinct table outlining their function and clinical significance before moving onto the mechanism. Although the ‘FGF Subtype’ table has proven to be effective and helpful, the table on ‘History’ does not seem to be thorough and is very limited. Possibly extending the table by researching more developments in the field of FGF Signalling could make it appear more complete.

Effort has been made to include a hand drawn image of the signalling pathway, which serves as a great source of aid in understanding how the pathway works whilst reading the text beside it. In saying that, effort should be further made to include a complete glossary and ensure terms such as ‘receptor dimerization’ ‘morphogenesis’ are broken down for the reader in order to satisfy criteria 4. This is not only seen in the ‘Signal Transduction’ section but also throughout the other sections. As you have included a fantastic image on bone development to represent the information visually, it would also be a good idea to post up images covering the other areas of embryonic development, such as kidney and inner ear development! You could even consider including short clips explaining these processes to make the page more interactive.

It is clear a decision has been made to talk about ‘Animal Models’. As well as including text on the topic, a possible option could be including a table briefly outlining which animal model has contributed to what knowledge in relation to the pathway in order to simplify the information.

A particular highlight of the Wiki page is the use of a quiz. It is great to see viewers can test their understanding of the topic towards the end and challenge themselves! For the correct option to each question a link to a supporting article or particular section of the page can be provided so the viewer can revisit the information should they have answered the question incorrectly. Overall a great use of tables, images and interactive components!

===Group 3 Peer Assessment===

With regards to your project I have noticed there are many forms of educational tools employed or being planned other than text, which to me is a big plus with regards to your project. The usage of the table to summarises the different FGFR sub-types is really easy to read and understand, and presents the information in a better way than you could’ve with just a wall of text. Your planned multiple choice section seems like it would be a nice addition to your page where it should help solidify the knowledge of the reader, allowing to check what they know. When doing the quiz section not only would it be good if you added explanations for the correct answers, but maybe also if possible explanations of why the other answers are wrong. There seems to be no issues with your citations given that all of them are in-text and multiple. Also the link between signal transduction, embryonic development and abnormalities is quite smooth and within context of their respective preceding parts, making the page read very well.

With regards to your usage of images, it seems mostly good and compliments the passages well, but I feel that it would benefit with adding more information to the legend, possibly by moving some of the description when clicking into the image into the legend. Also since your first image contains mainly abbreviations, maybe it would be good to collate all abbreviations and add it to the glossary such that the reader can easily refer to what the abbreviations mean.

With respect to your signal transduction section, all the components of the pathway seem to have been included, but for the most part how each factor interacts with one another has been left out. Elaborating on how each factor interacts and activates one another such as how FRS2 recruits GRB2 and SHP2, and how those events actually promote activation of RAS. I feel adding this will really improve the depth of this section, and make it less about a bunch of different components and more about how the work together in the context of their individual functions. Also I feel that the history section could be expanded on, maybe to include more time points or critical areas of discovery for the FGFR pathway.

Overall I think your project is shaping up quite well, and that with the addition of the suggestions made above, would make your project quite good. Having used many images, a table, and including the quiz has really made your page quite interactive and engaging which has really benefited your page. Also your subheadings and included passages have appeared to cover most important topics within your signalling pathway.

===Group 3 Peer Assessment===
Positive aspects of the project and improvements:

The group project looks terrific at the initial glance. You can clearly see all the headings and subheadings. In particular, it is great to see a range of subheadings such as “limb bud formation”, “bone development”, “kidney development”. This shows that there was a lot of research put into this project. Also by doing so you have made it clear that your project is about the Fibroblast Growth Factor Receptor Pathway (FGFR). The page is also very easy to navigate as well which was nice to see.
It is also great to see that there is addition of tables, images, and diagrams as it kept the read a lot more interesting and captivating. This allowed you to successfully satisfy criteria 2. It is also good to see correct in text citations and references as this allowed the reader to search for additional information if interested or necessary. Although you haven’t made up any multiple choice questions it is excellent to see a MCQ section. This is a great way to test the readers’ knowledge and in turn you can reflect if you have provided accurate and sufficient information to answer these questions.

It was great to see that you added an abnormalities section and in particular different types of syndromes and disorders. This meant that you went over the minimum information required and put in extra effort to create a coherent project. This satisfied criteria 5 and thus a better project. Overall there are many positives in this report and with minor amendments such as adding information to sections such as “Apert syndrome”, “Animal models”, “Kidney development”, “external genitalia development” etc, a very articulate and well rounded project will be created.

Negative aspects of the project and improvements:

Although there are many positives in the project, there should be some amendments to the project just to ensure all bases are covered. Firstly, it would be advised to increase the amount of information to the introduction and history sections. As these sections are lacking information, the reader may not have enough information to carry on reading as their base on this topic isn’t really strong and lacks information. This can easily turn off new readers and inhibit further exploration of the topic/ project. By adding additional dates in the history section, a better overall knowledge and background of the signalling pathway can be developed which can only enhance learning.

Overall, there are not many negatives and I believe as a reader your project was a great example of progress so far and with the aforementioned minor tweaks, your group is well on their way to achieving extremely high marks.

===Group 3 Peer Assessment===

Positive Assessment

Wow this is a very professional looking page and one that I was immediately drawn to. The introduction is very clear and simple and I was able to understand the basic of FGFR straight away which made it so much easier for me to try to understand the rest of the information. I absolutely love the use of the tables to introduce the sub-types of FGFR as this is so much easier to read than blobs of information. The dot points are concise and to the point and introduce each sub-type along with its abnormality.

The signal transduction in any signalling pathway is probably the most confusing and hard to understand part. However this part of your project is my favourite and I was surprised as to how quickly I managed to understand the molecular mechanisms of FGFR. The hand drawn diagram is amazing and really clearly displays all the key elements in play for FGFR. What I really like about your page is that it is really user and student friendly. It really invites learning and encourages it. The use of a quiz is a great example of this and really does allow the student to reflect on their knowledge.

Critical Assessment:

The page is absolutely amazing but in my opinion there are a few ways that it could be made even more amazing.

Sometimes the information is a bit overwhelming, in that there is too much of it. For example in the sections Limb Bud formation and Bone development, for information that complicated it would probably be better to employ the use of dot points or tables just to make the information more digestible. Although the hand drawing of the signal induction is extremely useful, I think it could be made even better by being accompanied with some specific step by step commentary which matches with the drawing. As a student this would make learning about FGFR a lot more engaging and easier.

The section on bone development although very informative could be more relevant to embryology and lastly a section outlining the treatments available for the abnormalities would be very interesting.

Overall great work guys !

===Peer Assessment: Project 3: Fibroblast Growth Factor Receptor (FGFR) Pathway===
====1. The key points relating to the topic are clearly described.====
The key points related to the topic are clearly described however the introduction is a little limited and further information is needed with examples.

====2.The choice of content, headings and sub-headings, diagrams, tables, graphs show a good understanding of the topic area. ====
The fibroblast growth factor receptor pathway wiki does overall seem to have a very extensive list of contents, which demonstrate that the topic is divided into clear interesting sections. This wiki has a good use of a table to demonstrate history (be it small) and subtypes of FGFR pathways.
In the history section it is not clear if they first discovered FGFR in human pituitary or pig or mouse. Please be more explicit. The history table does not seem to be finished as from 1999 to present there is no information at all added. Also there is no reference to the History information and this needs to be referenced.

====3. Content correctly cited. ====
The content is cited correctly. However as mentioned there are some sections which are not referenced at all: History, Bone Development (there is a large paragraph which says a lot of what is known but it is not referenced.
Some of the references are repeated in the reference list: see below in wiki guidelines.

====4. The wiki has an element of teaching at a peer level using the student's own innovative diagrams, tables or figures and/or using interesting examples or explanations. ====
There 2 small tables and two diagrams which are educational. I am very impressed that one of the members of the group re drew the first diagram. It is quite artistic but it is a bit confusing as to what each abbreviation in the figure means. If this sort of figure is added I think that some abbreviations or an explanation in the text needs to be added to allow the reader to understand what is actually happening . If not it looks like a figure with some sort of pathway but not very clear as to what It represents.

====5. Evidence of significant research relating to basic and applied sciences that goes beyond the formal teaching activities. ====
This is evident that the students have done a lot of research in this topic.

====6.Relates the topic and content of the Wiki entry to learning aims of embryology. ====
Yes there are some headings which relate to the learning aims of embryology such as limb bud formation and bone formation. But there are some sections which are not finished at all Kidney development, External Genitalia development, Inner Ear Development and Animal Models.

====7. Clearly reflects on editing/feedback from group peers and articulates how the Wiki could be improved (or not) based on peer comments/feedback. Demonstrates an ability to review own work when criticised in an open edited wiki format. Reflects on what was learned from the process of editing a peer's wiki. ====
It does seem that that the members of the group have had some communication and worked together well. It does seem that they have learnt to edit a wiki, making a online quiz, making tables, adding figures and content. Well done!

====8. Evaluates own performance and that of group peers to give a rounded summary of this wiki process in terms of group effort and achievement.====
This is a very interesting and well-researched wiki. There is still information lacking and more figures are needed as well as explanations for the figures. It is clear that a lot of effort has been carried out with the quiz, the figure that was re drawn from a publication.

====9. The content of the wiki should demonstrate to the reader that your group has researched adequately on this topic and covered the key areas necessary to inform your peers in their learning. ====
The key areas on this wiki have been researched adequately. There is still information missing.

====10. Develops and edits the wiki entries in accordance with the above guidelines. ====
Yes this wiki is in accordance with the guidelines. In terms of the reference list, some references have been re cited and added as new references, please see editing guidelines to avoid this- as so the reference is only listed once in the reference list and not multiple times.

===Group 3===
This page is developing well, as extensive headings have been well organised, with substantial written and visual information. A fantastic student produced image has been included, showing the different steps in the signalling pathway in a flowchart. It is very clear and neat, and the group is highly commended for this. An interesting and potentially humorous image can be included at the beginning of the web page to attract the reader’s attention and add interest to the page. Another image showing the ‘FGF and FGFR expression patterns during endochondral and intramembranous bone development’ has been included and is very clear and relevant. Another flowchart in the “Limb Bud formation” section would also help the reader summarise the different processes and the FGFR subtypes involved in each step. Adding short animations or movies would also be very helpful in aiding the reader understand these processes, particularly in the ‘Patterning Of The Embryonic Axis’ subheading. Images in the abnormalities sections, such as what the hands, broad thumbs, feet and medially deviated broad great toes of those with Pfeiffer Syndrome look like would also add depth to the web page.

Extensive and well organised headings have been included in this project, although some headings are still incomplete. A history section has been included in this web page. The timeline in this section requires more information as only two years, 1973 and 1999, have been included. More information is needed on the research carried out over the last decade, as well as gaps in this research, where future studies are heading and what is currently being researched in relation to this signalling process. The naming of researchers and where this research took place would also show depth of knowledge and extensive research, as required in the criteria. A heading at the bottom of the web page has been included titled “New and Emerging Research Into FG” and needs more information added to it. A summary of the current findings and research should also be added to the timeline higher up on the page when this section is further worked on.

Other sections including the glossary and “Animal models” sections have been started. Further terms to define in the glossary should include full names of terms such as RAS and AER included in the web page. The “Animal models” section is a comprehensive addition to the web page but is empty and requires further research. Ensure images of the animal models being explored are included in this section to enhance the textual information and to improve the readers’ understanding of these animal models. A table of the FGFR Subtypes has been included which is commended, however, needs much more elaboration as it is still quite bare. Images of these different FGFR Subtypes would also add depth to this web page.

In text referencing has been carried out well so far in this project. The writers often need to use references again when researchers and their research is mentioned again. For example, Mathias et al. (2001) is mentioned in the Subheading “Patterning Of The Embryonic Axis”. This research was referenced in the paragraph before the researchers were specifically mentioned, and thus should be referenced again with the same reference number. In the Limb Bud formation heading, a link to the lecture notes for Limb Development has been included. This is a very good way to allow the readers to easily access more information relevant to the topic.

GROUP 3

Overall from analysing through Group 3’s project I can starkly see that they have made a good attempt at addressing the marking criteria. The flow and clarity of the information in this project shows some serious thought and is showing a promising coverage of criteria 1. Not only this, but the group has excellently covered criteria 2 by having a plethora of headings, subheadings, tables and diagrams. Not only this but they have included a quiz which really shows an extra level of understanding and effort. One improvement that I might suggest is that they could extend the table by researching more developments in the field of FGF Signaling. Furthermore, this group has covered criteria 3 quite well as well but having a thorough amount of references and in text citations. Also, I have been able to learn a great amount of information from this project which means they have successfully achieved criteria 4. Overall, this project has done very well in presenting their project.
===Group 3 Peer Review ===
Group 3 has gathered a large amount of information and made good progress on the FGFR pathway, the introduction is well written and helps set the framework for the rest of the article. The organization of the page including the subheadings and formatting was very impressive and needs little work. The history section however should be attended to as there are only two entries, a more substantial history especially recent developments would be very beneficial in understanding the FGFR pathway.

The media usage is very abundant throughout the page and includes student made illustrations which is something many other groups have not yet incorporated thus is a very good sign. Of course more media could be used in the abnormalities section to demonstrate how these appear/how they are occurring..

Overall this group has done very well in addressing the marking guidelines once more content is added underneath the unfilled subheadings and the superfluous links/notes have been removed the article should come out very nicely.

===Peer Review===
The headings and subheadings on the page is used very effectively to aid the progression of information. Through the sequence of the headings, it allows the reader to build their understanding about FGFR signalling. The FGFR page definitely address the topic of this assessment - signalling in development, and links FGF signalling to a number of developmental events. This reflects the large contributions of FGFR in development which the page successfully portrays.

In the overview section, it states: “As shown in the image, an acidic box…”. Make it clear which image you are referring to because I can’t find it.

The table for the subtypes of FGFR has been acknowledged that it is incomplete but it gives a good snapshot to function and associated abnormalities of the different FGFR subtypes.

The page includes a student drawn image which summarises the FGFR signalling pathway. None of the other groups have included a student drawn image so good job! The images uses colours to distinguish particular molecules and shows the downstream signalling events to affect gene transcription in the cell. To me the image is a bit blurry on the page, so maybe change the pixels of the image to make it larger and easier to see?

The page includes a quiz which is clever and will definitely make the page stand out from the other groups.

Overall, Group 3 has made good progress. Good job!

Group 3: FGFR Pathway
Group 3, you have done an excellent job so far. Your page is well organized, with relevant headings of the topic such as ‘Role in Embryonic development’ and ‘Subtypes of FGFR’ that explore different elements of the FGFR pathway. A substantial amount of information is placed under the appropriate subheadings, which is good, however there are still a few where content needs to be added to improve the project. This page has a lot of potential and will be very informative once finished.

The introduction is very effective because it is short and succinct. It states what processes the FGFR pathway is involved in and mentions how it is involved in early development. There has been a good start to the history of the pathway. More dates and significant events, such as discoveries, should also be added here.
I like how you have included an ‘Overview’ of the pathway. It is a good reference point for students like me (who don’t know much about FGFR Pathway) to refer back to when content gets too confusing. In addition, the subtypes of FGFR were presented effectively through the use of a table. The organised structure of the table made it simple to understand, quick to read, and easy to compare the different subtypes. Well done!

Another positive aspect of the project is how you have incorporated pictures that support the content. I especially find the flowchart of the FGFR pathway very useful because it visually shows the process of the pathway. It is correctly citied and balances out the look of the page (instead of blocks of information in long paragraphs). In addition, I love how you guys have added a quiz. It offers something different to the project.
A good start has been made to the glossary. The purpose of a glossary is to simplify the meaning so that it is easier to understand. However, the definition was still a bit too complicated for me. Also, I suggest that more words should be added.
I was impressed by the use of in-text references throughout the project as it demonstrates that you have done significant research on this topic. The complete reference list at the bottom of the project contains a large number of articles, which is excellent. All articles used in this project have been correctly citied.
All in all, Group 3, you have done an amazing job! With a few minor tweaks and adding more information, I am sure that you will receive good marks for this project.

===Group 3 Peer Review===

Overall, it is a great page to look at with lots of information divided clearly into subheadings. The subtypes of the FGFR in the table is quite useful and clearly explain the differences between them, also the addition of the abnormalities in that table is very useful. The student drawn image is a very nice addition to the page, however some of the writing is slightly difficult to read. The section on the role on embryonic development is quite detailed and very well set out. There are many reference throughout the page, which is very useful to the reader. The abnormalities are discussed very well and you have explored a large range of possible abnormalities.

The history information is lacking a little and doesn’t provide much understanding on the progression of knowledge on this topic. The overview of the pathway is quite simple, so I don’t feel like I have a good enough understanding of what the pathway actually entails. You should probably include a better glossary section as you have a lot of complex terminology within the page that is not explained, so a glossary list will help the reader better understand what is going on. The section on bone development is slightly confusing due to the image used. The image is very complicated and has a lot of detail within it. One change would be to draw the image yourself to simplify it and express only the information required. There are a lot of blank sections within the page that will hopefully be filled in soon.

The addition of the quiz at the end of the page is a very nice idea, however, I was disappointed to see that both the questions and answers were still blank. I do really like the idea of it and I feel that once it has been finalised it will be useful to the reader.

Looking at the page as a whole, I really like the way everything is set out and the content you have covered. Most of the information is very clear to understand and some of the images compliment the writing very well. Some small changes can be made to assist the understanding of the reader.

===GP3 peer review===

Introduction had explained what does this signalling pathway do and importance and page outlining. Followed by history part but seems more would be added. Pictures and table are used to assist explanations. Detailed content but seems need sub-heading or spacing ( formatting). Some gap parts are found. If the abnormality could be linked to the table above would be better. Quiz part is made but needs questions. Some pending glossary are found. Good references formatting.

==Comments by Group 3==

[[User:Z5015686|Z5015686]] ([[User talk:Z5015686|talk]]) 12:36, 19 August 2016 (AEST) I thought looking into how prenatal cannabis exposure influences signalling during development might be interesting

[[User:Z5017002|Z5017002]] ([[User talk:Z5017002|talk]]) 12:47, 19 August 2016 (AEST) Ooh cool idea, I agree that looks really interesting, there seems to be a lot of literature about its influence on brain development

[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]])z5015544[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) Thats excellent, what about the sonic hedgehog pathway?

[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]])Other ideas[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) WNT Signaling Pathway is another one to look at

How can we harvest stem cells from the embyro for use in later life - z5015337

[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]])z5015544[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) Ok guys I created a couple of subheadings and provided a brief history. Make sure to use primary research articles that are peer-reviewed because I just spoke to Dr Hill and noticed he stressed that a lot.

[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]]) I have scoured through the projects of old to get a better idea about what is expected from us for this project - [[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]])

[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]])I found this giant slab of text regarding the structures of the receptors involved from a journal article and I am working through culling it down for a usable structure definition: FGF receptors and FGF signal transduction. FGFRs are modular proteins comprising 3 immunoglobulin domains (IgI, IgII and IgIII). IgI and IgII are separated by an acidic box (AD). IgII contains a heparin binding domain (HBD). The IgIII domain is followed by a unique transmembrane (TM), a juxtamembrane (JM) and a kinase domain (KD) interrupted by an interkinase domain (IKD). FGF ligands linked to heparin sulfate proteoglycan (HSPG) bind to IgII and IgIII of FGFR. This results in the dimerization and the subsequent transactivation by phosphorylation of specific tyrosine residues. The main two transduction pathways involve the phospholipase C-γ (PLCγ) and the Ras/MAP kinase. The SH2 domain of the PLCγ interacts with the phosphorylated Y766 of the activated receptor. The activated PLCγ hydrolyzes the phosphatidyl-inositol-4,5-diphosphate (PIP2) to inositol-1,4,5-triphophate (IP3) and the diacylglycerol (DAG). IP3 releases Ca2+ while DAG activates the protein kinase C-δ (PKCδ). Activated PKCδ activates Raf by phosphorylating its S338 and stimulates the downstream pathway in a Ras independent manner. The main pathway involves the interaction of the docking protein FRS2α with the amino-acid residues 407–433 (Xu et al., 1998). This protein is activated by phosphorylation on multiple tyrosine residues and subsequently interacts and activates Grb2 linked to Sos, a nucleotide exchange factor involved in the activation of Ras. Activated Ras then activates Raf which stimulates MEK which in turn phosphorylates the MAP kinase ERK. This last activated component translocates to the nucleus and phosphorylates specific transcription factors of the Ets family which in turn activate expression of specific FGF target genes. P: phosphorylation

[[User:Z5015686|Z5015686]] ([[User talk:Z5015686|talk]]) 18:31, 14 September 2016 (AEST) Hey guys I've just changed our subheadings so we can better allocate something for each of us to write on this week. More then happy to change them! Just came across these while I was researching. Did everyone maybe want to put their name next to something they are able to research or chuck in new subheadings that interest them?

[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) 14:31, 16 September 2016 (AEST)Hey guys, here is the link for omim. Type in the name of the gene and it will give you different articles about it: http://www.omim.org/[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) 14:31, 16 September 2016 (AEST)

[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) 14:41, 16 September 2016 (AEST)Things to include: Flow diagram of the FGFR pathway, 3D diagram of the FGF protein (can be hand-drawn)[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) 14:41, 16 September 2016 (AEST)

[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) 23:22, 28 September 2016 (AEST)Hey guys, hope you're all enjoying the break. Just thought I would let you know I've added a hand drawn diagram and a table too. If anyone finds more information about specific receptor functions in embryo development please add it to the table.[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) 23:22, 28 September 2016 (AEST)

[[User:Z5015686|Z5015686]] ([[User talk:Z5015686|talk]]) 12:35, 29 September 2016 (AEST) '''just moved this from our main page''' Extra Resources
Useful review articles that may be worth a read through:
http://onlinelibrary.wiley.com/doi/10.1002/wdev.176/full
http://www.nature.com.wwwproxy0.library.unsw.edu.au/nrd/journal/v8/n3/pdf/nrd2792.pdf
http://www.sciencedirect.com.wwwproxy0.library.unsw.edu.au/science/article/pii/S0012160605006184
http://www.nature.com.wwwproxy0.library.unsw.edu.au/nrm/journal/v14/n3/full/nrm3528.html
http://onlinelibrary.wiley.com.wwwproxy0.library.unsw.edu.au/doi/10.1002/jcp.24649/full
http://genesdev.cshlp.org/content/29/14/1463.full (FGF signalling and skeletogenesis, specifically how mutations to the FGF signalling pathway may be responsible for skeletal diseases)

[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) 01:14, 4 October 2016 (AEDT)Looking really good guys, I think we should try and expand beyond what has been covered in the lectures. Maybe we can look at new research involving FGF. We can also look at FGF in animals and how it affects limb development. Let me know what you guys think
 
[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) 13:18, 7 October 2016 (AEDT)http://www.sciencedirect.com/science/article/pii/S0925477397006679[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) 13:18, 7 October 2016 (AEDT)

[[User:Z5015686|Z5015686]] ([[User talk:Z5015686|talk]]) 13:14, 16 October 2016 (AEDT) Just fixed up our references so they aren't listed multiple times, and added an automated search on pubmed for extra information. I think the videos and pictures are a nice addition, and agree its a good idea going beyond the information covered in the lectures. I might also add links to omim for further readings into abnormalities. I think animal models is important to include so FGF in limb development is a good idea. I was also thinking of adding some coloured text just to break up the information a little if that sounds okay?

Ignore this for now guys, this is more for external genitalia bits I might want to add
Tissue-specific roles of Fgfr2 in development of the external
genitalia - Include the glossary definition for hypospadias or explain it within the text.

[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]])Proofread the wiki![[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]])

2016 Group Project 3

2016-10-22T04:16:54Z

Z5015337: /* Fibroblast Growth Factor Receptor (FGFR) Pathway */

2016 Group Project 3

2016-10-22T03:41:43Z

Z5015337: /* Fibroblast Growth Factor Receptor (FGFR) Pathway */

Talk:2016 Group Project 3

2016-10-17T11:26:35Z

Z5015337: /* Comments by Group 3 */

2016 Group Project 3

2016-10-17T11:22:52Z

Z5015337: /* External Genitalia development */

2016 Group Project 3

2016-10-17T11:20:50Z

Z5015337: /* External Genitalia development */

Talk:2016 Group Project 6

2016-10-07T01:54:40Z

Z5015337:

{{ANAT2341Project2016discussionheader}}
=Peer Review=

===Group 6===
Good try group 6. Key points appear to be well selected, however perhaps consideration of clinical aspects of your research could be considered useful. Your subheadings should be fixed so that all of your information does not come under the introduction section and also perhaps include more pictures in your project. You guys have a good lay out of information, now you really just need to fill those sections up with information, definitely have a sound understanding of the topic area. There are little to no references as of yet and none of the references in the references section have been cited correctly, this can be fixed by simply using the inbuilt referencing mechanism we have been using for our weekly assessment items. Also, more peer reviewed journal articles should be used and cited to provide authority to your information.

The information presented is very peer friendly and understandable but will need the inclusion of hand drawn diagrams to satisfy this criterion completely. There is not much evidence to suggest that your team has went beyond the formal teaching activities, perhaps incorporate a video or quiz into your work. In terms of the course aims of embryology, you have not satisfied the second criteria regarding new technology/current research as of yet and have vaguely addressed the key criteria regarding TGF and embryological development.

Overall, the areas to be discussed appear to be sound but need to be edited so that the information will flow better. Your team needs to put more information into each section, I would recommend looking at some of the other teams to see how much information is seemingly adequate. Ensure that you reference your information correctly and you should be good when you guys put more research onto your page. Good luck and nice
try!

===Group 6 Peer Review===
Group 6 - it looks like you’ve started off well and from the headings/subheadings you’ve chosen, I think you’ve chosen some great aspects to explore. The content you have so far is relevant and written in a way that’s easy to understand. Your explanation of the signalling pathway is good and you’ve included some pictures, but I think more work still has to be done.

Your page is clearly still being worked on but here are my suggestions. Firstly your page really needs a lot more content. You haven’t explained anything about the involvement of TGF-beta in embryonic development yet and that’s supposed to be the key point of this project, so you should really focus on finding some info about that. Your referencing as well is really poor. Make sure you have in-text referencing so that the reader knows exactly where each part of your content has come from - at the moment there are no clear references for anything you have written. You should especially be referencing your images (in the image caption). You should also edit the formatting of your headings because at the moment they are all considered subheadings of ‘Introduction’. I would suggest moving the history section to the beginning of your page and presenting the info in a table. And it would be really great if you had a section on ‘Animal Models’ and ‘Abnormalities’, like most of the other pages have done. Your references section is also not formatted correctly so you need to fix that. As long as you work hard from now on I think you can still put up a great project!

===Group 6 Peer Review===

'''Positive Factors'''

Group 6 have shown that they intend to cover the scope of the topic by the subheadings they have added to their page so far (which will allow them to adequately address criteria 1 and 2). The explanations so far are easy to understand from a student’s perspective, and have supporting diagrams to support the information on TGF (which shows they have begun to address criteria 4). Another strength of this page is the inclusion of a ‘Further Reading’ section, which could allow readers to access more relevant information if they wish to do so.

'''Points for Improvement'''

Some improvements that Group 6 could make to their page are as follows: Group 6 could format the subheadings so that they do not all fall underneath ‘1.1 Introduction’; furthermore they could add in-text referencing with numbers that link to a ‘References’ section at the bottom of the page; and also Group 6 could improve the formatting of the images to be more incorporated into the flow of the page.

'''Overall'''

Overall I think Group 6 have formed a good template to add more information on the scope of their topic, and have begun to address some of the criteria. Most importantly I think they should try and address criteria 5 and 6 more adequately, and make a couple of formatting changes to the page so that their well-written explanations are more engaging and organised for a student audience.

 
 
Group 6:
 
 
Positive aspects of the project and suggested improvements:
 
 
The authors of group 6 have created a variety of subheadings related to the TGF-beta signalling pathway, including the nature of the growth factor, its mechanism of action, history and emerging research (criteria 1). Authors have also provided two diagrams related to TGF-beta signalling which reinforces the description of TGF signalling provided (criteria 2). These diagrams allow for a much simpler interpretation of the signalling process described and assist in teaching at the peer level (criteria 4). It appears that the authors are beginning to conduct investigations into new research surrounding TGF-beta signalling, thus indicating that they are attempting to research beyond formal teaching activities (criteria 5).
 
 

Whilst it is excellent that multiple subheadings have been provided, a possible improvement would be to include a much larger variety of subheadings which cover the scope of TGF-beta’s role in embryonic development, abnormalities, types of TGF receptors and animal models. This may allow audiences to understand the big picture surrounding this signalling pathway which will assist in the understanding of the information already provided. Another improvement to this page would be to include more images under different subheadings. One example would be to include an image or table showing the history of discovery surrounding discovery of this signalling pathway.
 
 

Negative aspects of the project and suggested improvements:
 
 

Although there were positive aspects of this project, there were also numerous negative aspects which may be improved. One key negative feature of the page was that the authors did not discuss the role of TGF-beta signalling in the context of embryonic development, hence meaning they failed to meet criteria 6. To ensure that this criterion is met, authors may conduct research into the involvement of TGF-beta in specific processes that occur during embryonic development, perhaps organ development and growth of different primitive structures. In addition, whilst the authors have provided a history of the TGF-beta signalling pathway, the history appears to be very brief. Thus an improvement which may be implemented would be to include a more extensive background regarding the history of discovery of the pathway. It was also noticed that no tables were utilised within the page. A possible improvement would be to include a table describing different abnormalities and their causes in the context of disruption of the TGF-beta pathway. A table may also be utilised to describe different subtypes of TGF-beta receptors as well as their functions during embryonic development. Tables may be utilised as they will assist in the process of teaching at the peer level (criteria 4), particularly because they convey information in an orderly and organised manner.
 
 

The authors of this project also failed to meet criteria 3, in that only one source was referenced in the process of the signalling pathway and also no in-text citations were provided. In addition, authors failed to reference the image file named, “Process of TGF-beta signalling pathway 01”. It is vital that all sources are referenced correctly in order to ensure that the copyright laws regarding the use of information are adhered to. The final negative aspect of the project was that the page did not flow very well, in that subheadings were arranged in a disorderly fashion. An example of this is the inclusion of the subheading labelled, “history of TGF-beta signalling pathway”, towards the end of the page. Since such a subheading provides a background surrounding the pathway, a possible improvement would be to include this subheading at the beginning of the page. By ensuring the orderliness of the page, this creates a sense of coherency between subheadings, thus making the page more appealing and engaging.

===Group 6===

It was good to see some progress being made on the project with the development of some subheadings and the inclusion of an image. In saying this, a better selection of headings and sub-headings could be developed to break down the topic of TGF beta signaling pathway. I think the sub-headings provided under the general heading of ‘Introduction’ could form the main headings of this research project and they could then be further broken down into various subheadings. In addition, the subheading of TGF-beta could be eliminated and this definition could be incorporated into the glossary or general introduction of the topic instead. Furthermore, more focus is needed on the influence of this pathway on embryological development and the abnormalities caused by mutations to the pathway and its components. For example, there has been mention of the effect of TGF-beta in ‘development of the embryo and adult organism, as well as cell growth, immune function and hormone secretion’ but further discussion has not been pursued.

Though a good description of the ‘process of TGF-beta signaling pathway’ has been provided, it could be further improved by referencing the images included in this section in your text (e.g. refer to Figure 1) to aid one’s understanding of the concept being explored. In addition, a timeline of events could be provided to explore the history of this pathway and it would be appropriate to begin with the discovery of TGF-beta. To a reader, information on ‘transformed or malignant cells’ seems unrelated to the TGF-beta signaling pathway even though it may be in fact be related, due to lack of discussion of this pathway or TGF-beta in this description. In regards to the section on ‘Limitations’, what types of limitations are you trying to explore? Limitations in research? This could be better defined by appropriately allocating subheadings to each of the sections.

Though you are heading in the right direction, spending time to produce a basic layout of your project by creating appropriate headings and subheadings would be useful in breaking down the concepts needed to be explored in this pathway. This could be achieved by communicating with group members through the discussion page and providing feedback and suggestions. In addition, greater focus is required in referencing and citing your work to ensure researchers and authors are acknowledged for their work. Also, by exploring animal models of the TGF-beta pathway and the effect of this research in understanding this pathway in humans and its influence on embryological development, you could greatly increase the quality of your work. You could also try and make your project more interactive and engaging through the inclusion of tables, images and diagrams. I hope this helps! Good luck!

=== Group 6 Critical Assessment===
It is great to see an in-depth overview of the TGF beta Signalling pathway and it’s mechanism of action. The page is off to a great start and with a few key improvements it can turn into a successful one! Firstly, I like the use of images to aid the reader in understanding the content better should they be a visual learner. By reading the text on the way the pathway works, it is clear it is a complicated process hence a suggestion would be to add short clips/animations to simplify it for the viewer.

Under your introduction an attempt has been made to briefly highlight the main features of the pathway, however a negative of this section is that a lot of the content is basically listed. For example it is mentioned TGF-beta is part of a larger TGF superfamily comprising of different members such as activins and GDFs. Instead of listing, try presenting your information in a different format such as a table with s few columns stating the member, it’s function, and possibly what a mutation could lead to.

Additionally it is also stated that TGF beta has certain functions such as controlling angiogenesis however doesn’t expand on the ‘other’ functions it has. To turn this into a positive, dedicate different sections on how the pathway is involved in angiogenesis, hormone secretion, proliferation etc. If there are too many functions to fit onto the page, you could shift a few to your ‘Further Reading’ section as an option if the reader would like to explore further into the pathway’s functions, or construct a hidden table that the viewer can expand if they wish to.

In order to satisfy criteria 3, in text citations should be incorporated within text so the viewer has an option to access the article if they find the statement interesting. A reference list has been posted with a few references however ensure they are cited in the correct format. Overall a great start!

===Group 6 Peer Assessment===

In this project page a good start has been made with the inclusion of images to compliment the signalling pathway description. Appropriate abbreviations appear to be used, where the full name is used first. Also the additions of a glossary and further reading subheading is a nice touch, which should allow for better understanding of the topic should the reader want more information. In terms of the diversity of the subheadings though, it seems that a lot more could be added, such as animal models used to research the signalling pathway and also possibly abnormalities that may arise from the errors or mutations in the pathway. It is probably wise to also add a section regarding embryological development and what role TGF beta signalling pathway has in it, which should help provide context to the abnormalities section when added.

The usage of pictures is appropriate for the section it has been put in, and compliments the signal transduction pathway description well, but the picture labelled “Process of TGF-beta signalling pathway” does not appear to be referenced or have the appropriate copyright under it. There is also no legend for this picture to briefly describe it. Also for most of the page there are limited to no references, where for the signalling pathway section, it appears your groups has used websites rather than peer reviewed articles as a source. The websites are probably good starting points to get a general idea of the pathway, but it is probably better if you find peer reviewed papers to cite, which potentially the websites you have used have cited. Also when citing it is best to use in text citation such that the reader can easily see which paper you are referring to when describing certain facts.

Also in your groups signalling section, it is mentioned that SMAD when activated, recruits various transcriptional regulators that control expression of numerous genes. This is quite vague and is probably a good idea to mention some of these factors, and also what genes they regulate and the importance of such genes. Doing this should also provide your group with a good link to the embryological development section with regards to TGF-beta signalling.

It still seems that overall there is a lot of work to be done on your groups page, but a good start and effort has been made to include various images and also subheadings. I feel that if your group incorporates some of the suggested subheadings described above, and other feedback mentioned, the page should be greatly improved.

===Group 6 – TGF-beta===
You guys have made a good start to the project identifying some important subheadings introducing the TGF-beta signaling pathway, outlining its history, current research and limitations (which may be more appropriately labeled as abnormalities.) However, I do think the structure of these should be revised, what I mean by this is that you should create more levels of headings (as currently all the headings are located under the larger heading of introduction.) Furthermore, it terms of the headings, I think you need to introduce the signaling pathway, then discuss the history of its discovery, then discuss the specific mechanisms behind the pathway, its role in embryonic development (which is a very important aspect in order to relate your project back to what we are learning in the lectures and tutorials), then animal models and abnormalities. You have chosen to include some images which appear to be useful for explaining the signaling pathway, however I think it is important to refer to them in your text, as well as appropriately referencing them with the copyright from the original source (as the larger one is missing this information.)

Some negative aspects of this project are the lack of appropriate references, there are no in-text citations and the identified sources that have been used appear to be websites. Remember that most of the information, if not all should be acquired from primary research articles (supplemented with the occasional review article.) Furthermore, similar to other projects, in order to make your page more engaging you could look into including tables (say for the history or summary of receptor subtypes), more images, YouTube links or animations, or an interactive quiz.

In conclusion it seems that there is still a lot of work to be completed on this page before it is to be submitted, however you have made a successful start. The main criticisms are regarding revisiting the subheadings and including the role of embryonic development as I think this is really critical to the project, as well as adding more information to the page in general. In saying that it appears you guys are heading in the right direction!

===Group 6 Peer Assessment===

Positive aspects of the project and improvements:

Upon reviewing the page I can see a number of headings and subheadings such as the nature of the growth factor, its mechanism of action, history and emerging research. But to be critical, a range of other headings is necessary to ensure all bases are covered when researching and providing the relevant information. This will help in satisfying the requirements for criteria 1 and 2. It is good to see the addition of a diagram to your project as it is a requirement for criteria 2. This provided a visual aid that kept me interested to find out more about the topic while simultaneously making it easier to understand the theory behind the process of TGF Beta signalling pathway. It is also great to see the current research and limitations as this shows that you are going beyond the scope of the required criteria and researching ahead to provide that extra bit of information. This in turn is a great way to satisfy criteria 5.

Negative aspects of the project and improvements:

Although there are a few positives in the project, there are a number of negatives which can be improved upon to ensure a coherent project is created. Firstly, it is advised to put the heading “history of TGF- beta signalling pathway at the top” with the introduction as this is an introductory section and should be addressed initially on the page. This will allow you to create a more flowing page which also looks nice. Secondly, it would be advised to add more images and tables as it is a requirement for criteria 2. By doing this you will keep the reader engaged and wanting to find out more about the chosen topic. In saying that, you already have a couple of images but not referenced. It is imperative to correctly cite and reference these images as failure to do so will result in a breach of copyright laws.

Another critique is to add more subheadings with a range of different aspects of the signalling pathway being explored. It is recommended that you dedicate a chunk of your project to describing the pathway in detail and its role in embryonic development and abnormalities relating to mutations caused by the pathway. This will ensure you answer criteria 6 as it is a great deal of the report. It is also advised to put the history section under the introduction section as placing it in the middle of the project is a bit out of place and inhibits the flow of the information from one subheading to another. Also, the history section can be improved by adding more information as there have been more findings in this research topic since the 1970s. An addition of glossary is also needed for terms such as “peptide”, “cytokine”, “angiogenesis”, “protein kinase” etc. This will aid readers understand terms that they previously have not encountered and allow them to correctly understand the context of the information.

It has also come to my attention that there are little to no references or in text citations. By adding information without correctly giving the authors credit is a breach of copyright laws and must be done urgently. Overall, the project shows signs of progress with a number of positives. By reflecting on the negative aspects and acting upon it, it is certain that high marks are in order.

===Group 6 Peer Assessment===

Positive Feedback:

The introduction is very simple and clear making it a perfect way to familiarise with the TGF-beta signalling before diving into any more information.
The process is also described very well as it is aided with two pictures which were excellent choices. Together the information and the pictures collate to create a stable understanding of how TGF-beta signals actually communicates.

Critical Feedback:

You guys can definitely focus on explaining its role specifically in embryo development which is a key criteria for this project. This can be done in many was such as tables or pictures if there is too much information. It would also be a good idea to talk about the things that could go wrong with TGF-beta signalling pathway and the current research being done to rectify this as this is something that is very interesting and also relevant.

You guys should also start referencing early as it can become very problematic later on to keep track and doing very quick citations would go a long way later when editing the project. Lastly it would possibly help if everyone brainstormed some subheadings and categories that you further want to talk about e.g. animal models and that way you know what information you are looking for.
This page has a very strong start and if that quality is carried through to the rest of the content it will be a very successful page.

=== Group 6===
This web page is slowly developing, and in comparison to the other web pages, is lacking in information, meaning there are many improvements that must be made before submission. Headings have been included which are relevant and cohesive. However, the information beneath these headings should be more substantial in text and images. Two comprehensive diagrams have been included, however they are not properly labelled or referenced. Including student drawn diagrams, tables or figures would be a great addition to the web page and would fulfil the criteria for including student's own innovative diagrams, tables or figures and/or interesting examples or explanations. The images included would serve better further down in the web page where the reader has knowledge of this signalling process and what is involved to then apply and consolidate in the image. When they are placed so high up in the web page before the reader has learnt about the process, it often makes the images seem irrelevant until this information is read. Seeing terms for the first time on an image is not the purpose of a diagram. Rather, they should consolidate and summarise the information that has just been read. Other inclusions could be a video or short movie showing processes discussed, such as the bone and cartilage formation, mesoderm induction and patterning and dorso-ventral patterning controlled by the TGF superfamily.

Several things could be included to make this web page more substantial. A table comparing and summarising the different members of the TGF family would add to the depth of this page. This table would compare the family members: TGF-beta 1, 2 and 3, Activins, Inhibins, Lefty, Nodal, Growth Differentiation Factors (GDFs), Bone Morphogenetic Proteins (BMPs), Glial-derived Neurotrophic Factors (GDNFs) and Mullierian Inhibiting Substance (MIS). This would provide evidence of significant research, which would satisfy the criteria of this project. Many of the headings and sections have not been completed. For example, a glossary section has been started but needs to be more substantial. This could include more terms such as explanations for the abbreviations used in the first diagram at the top of the page - LTBP1, LTBP2, LTBP3, LTBP4 and more.

A “History of TGF-Beta signalling pathway” has also been included with minimal information. This section would be made more accessible and easier to read by arranging it on a timeline. A “Current research” heading has also been added but again needs more information. This section is important as it highlights current gaps in knowledge. It should also be summarised to be included in the “History of TGF-Beta signalling pathway” timeline. The “Limitations” heading is not very clear. Changing this title to “Abnormalities” or something similar would be more relevant, and again more information is needed to enhance the reader’s understanding of the topic. Images could also be included here to describe the symptoms or characteristics of the diseases associated with Mutations in the TGF-beta RII gene.

Many improvements can be made to the referencing of the information in this project. No in-text referencing has been included. A few internet links have been placed under a “References” heading. This is not sufficient as the reader does not know exactly where each piece of information has come from, and hence are not able to search for the exact research paper for more information on a specific section. A wider range of references would also show comprehensiveness in the research of the group, and that they have widely researched this topic, again satisfying the criteria of this project.

===Peer Assessment: Project 6: TGF beta Signaling Pathway===
====1. The key points relating to the topic are clearly described. ====
There are headings for key points but the information for these key points has not been added so far. There is a heading for introduction but this has not been filled.

====2.The choice of content, headings and sub-headings, diagrams, tables, graphs show a good understanding of the topic area. ====
There are two black and white figures which are quite clear and well done. However they are not referenced.

====3. Content correctly cited. ====
The content is not cited correctly. There is a reference section but there are no publications that have been cited listed. The figure is not referenced at all. If there is any information on the page why are there no citations at all????

====4. The wiki has an element of teaching at a peer level using the student's own innovative diagrams, tables or figures and/or using interesting examples or explanations. ====
There are two figures. There does not seem to be any examples or explanations that show the students own innovation. A time line would help a great deal.

====5. Evidence of significant research relating to basic and applied sciences that goes beyond the formal teaching activities. ====
This is somewhat evident but there is not enough clear information and it makes it difficult for the reader to follow the topic. There are only a few topics which have information. Clearly not enough work has been done by the students.

====6. Relates the topic and content of the Wiki entry to learning aims of embryology. ====
Yes there is some information, which relates to the aims of embryology. However so much more is needed. The introduction has some information on how TGF beta controls certain processes in development such as proliferation, cellular differentiation, angiogenesis etc however this needs to be clearer. I am not sure where the introduction finishes and new sub headings begin.

====7. Clearly reflects on editing/feedback from group peers and articulates how the Wiki could be improved (or not) based on peer comments/feedback. Demonstrates an ability to review own work when criticised in an open edited wiki format. Reflects on what was learned from the process of editing a peer's wiki. ====
Each section has been divided amongst the group but it seems that the members of the group have not really communicated or finished their own sections. This is not clear at all. There is no communication in the Discussion section.

====8. Evaluates own performance and that of group peers to give a rounded summary of this wiki process in terms of group effort and achievement.====
This is not demonstrated and it seems that the key areas have not yet been researched adequately. There is still a lot of information missing and the overall flow of this wiki is a work in process it seems. There is no information discussed between the students in the Discussion area.

====9. The content of the wiki should demonstrate to the reader that your group has researched adequately on this topic and covered the key areas necessary to inform your peers in their learning. ====
The key areas on this wiki have been set up but there is no clear and adequate information that is correctly cited at all. It is a very poor effort thus far in terms of group research. Nothing has been cited correctly.

====10. Develops and edits the wiki entries in accordance with the above guidelines. ====
This still has not been achieved at all. There is no editing and it seems the group has put little effort in this project.

User:Z5015337

2016-10-07T01:53:47Z

Z5015337:

{{ANAT2341Student2016}}
==Lab 1 Assessment==
<pubmed>26446757</pubmed>

In the aforementioned research article, the "Onobrychis Viciifolia" or rather, sanfoin is explored in detail with respect to its ability to self fertilise and therefore be a sustainable and useful plant for its local ecosystem. This is due to its ability to reduce the need of nitrogen fixation by bacteria as a Legume. On top of this, Sanfoin has tannins in it that assist with the break down of proteins and as such, it is beneficial to animals.

This research article utilises naturally directed pollination and artificially directed pollination to compare rates of self fertilisation. Interestingly, the plants of sanfoin that used artificially directed pollination had much higher rates of self fertilisation than the natural counterpart. Whilst there are other results obtained, these are the main results that by implication indicate that we can assist the growth of local plant systems by artifically pollinating sanfoin, which will provide nutrients and reduce the dependence on nitrogen fixation for plants to obtain nitrogen.

{| width=95%
|-bgcolor="FAF5FF"
| [mailto:m.hill@unsw.edu.au Mark Hill] 18 August 2016 - You have added the citation correctly and written a good brief summary of the article findings. However, a plant study on "fertilisation" is not really what I was asking, in particular as this is not a Botany course, please try and focus on course content.

| width=100px| Assessment 4/5
|}
==Lab 2 Assessment==
[[User:Z8600021|Mark Hill]] ([[User talk:Z8600021|talk]]) 10:17, 19 August 2016 (AEST) you need to use the full file name (.jpeg).

[[File:Extracellular calcium levels compared to Spermatozoa levels.jpeg]]

Effect of extracellular Ca2+ depletion on the human zona pellucida-induced intracellular [Ca2+] increase in spermatozoa<ref><pubmed>PMC1712232</pubmed>
[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1712232/]</ref>

{| width=95%
|-bgcolor="FAF5FF"
| [mailto:m.hill@unsw.edu.au Mark Hill] 29 August 2016 - All information Reference, Copyright and Student Image template not included with the file and citation not referenced on your page here. I cannot complete the assessment without knowing the original source (reference for this image). Please update so that I can complete the assessment.

| Assessment ??
|}
===Lab 3 Assessment===
{| width=95%
|-bgcolor="FAF5FF"
| [mailto:m.hill@unsw.edu.au Mark Hill] 29 August 2016 - Quiz Mesoderm and Neural

| Assessment 5/5
|}

===Lab 4 Assessment===
====Gastrointestinal Tract Developmen====
.

<quiz display=simple>

{The mesoderm consists of epithelium, connective tissues, blood vessels, mesentry, smooth muscle.
| type="()"}
-   true
+   false
|| Whilst the mesoderm consists of connective tissues, blood vessels, mesentry and smooth muscle, epithelium is located in the endoderm and not the mesoderm .





{Select the most correct option of the following options:
|type="()"}
-   The superior mesenteric artery supplies the hindgut
-   The foregut is suppled by the inferior mesenteric artery
-   The celiac artery supplies the midgut
+   The superior mesenteric artery supplies the midgut
||The superior mesenteric artery supplies the midgut, the celiac artery supplies the foregut and the inferior mesenteric artery supplies the hindgut.



{Which of the following statements about lumen abnormalities are correct:
|type="[]"}
-   Atresia is a term that refers to the narrowing of the lumen
+   The formation of parallel lumens is a form of stenosis
+   An abnormality that results in interruption of the lumen is Atresia
-   Duplication results in perpendicular lumen
|| The key to solving these sorts of questions are to ensure that the questions are read carefully as there is usually a trick in the wording. Atresia refers to an interruption of the lumen, not narrowing of the lumen. Parallel lumen formation is a form of specialized stenosis. As mentioned prior, Atresia refers to an interruption of the lumen. Duplication will result in the formation of parallel lumens and not perpendicular lumens.

{Select the most correct option of the following options in the context of patterning signals:
|type="()"}
-   Endothelin is expressed in the anterior part of the primitive gut.
-   Cdx2 regulates the migration of enteric neural tube cells
+   GDNF regulates the migration of enteric neural crest cells
-   Sox2 is expressed in the posterior part of the primitive gut.

||Endothelin regulates the migration of enteric neural crest cells/ Cdx2 regulates the migration of enteric neural CREST cells, not tube. GDNF regulates the migration of enteric neural crest cells. Sox2 is expressed in the ANTERIOR part of the primitive gut.

</quiz>

==Lab 5 Assessment==
I have completed the prescribed questionnaire during lab.

==Lab 6 Assessment==
1. A known genetic mutation that is associated with cleft lip is the mutation of the p63 or TP63 which allows the encoding of the Tumour protein p63.

2. A research article that explores this gene is:

<pubmed>2564545</pubmed>

3. Mutations of the p63 gene are detrimental as it is a critical regulator that prevents a host of defects in development, such as ectodermal dysplasia. Without the presence of this gene in mice, the mice died at birth and had truncated limbs as well as epidermal defects<ref><pubmed>16524929</pubmed>[http://www.ncbi.nlm.nih.gov/pubmed/16524929]</ref>.

In the context of cleft palate syndrome and the p63 gene, there is not a clear reason as to why mutations of the p63 gene can result in cleft palate but as cleft palate is a form of ectodermal dysplasia and functioning p63 prevents dysplasia, a connection can be made <ref>[https://ghr.nlm.nih.gov/gene/TP63#conditions]</ref>.
==Lab Attendance==
[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]]) 9/09

[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]])23/09[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]])

==Lab 7 Assessment==
1. The dystrophin gene is located on the locus of the X chromosome and is responsible for the transcription of dystrophin. A mutation of this gene will therefore result in altered expression of the muscle isoform, dystrophin<ref><pubmed>14636778</pubmed></ref> . Mutations like these can result in Autosomal recessive muscular dystrophy and Duchenne and Becker muscular dystrophies to name a few.

2. Dystrophin is a critical protein that is responsible for linking the actin filaments to the sarcolemma, which is a protein that is located in the interior of the plasma membrane of individual muscle fibres<ref><pubmed>11917091</pubmed></ref>. Dystrophin is critical in ensuring the stability of muscle fibres and without it intracellular calcium handling is altered resulting in muscular function being impaired<ref><pubmed>15470384 </pubmed></ref>.

3. Other organs that are affected by this disorder are the heart and those responsible for respiration as there is gradual loss of healthy muscular fibres which by cellular repair mechanisms are replaced with inelastic fibrous tissue resulting in less effective contractions resulting in cardiac and respiratory failure<ref><pubmed>4767260</pubmed></ref> .

4.

5 The animal models available for muscular dystrophy are historically the MDX mouse and more recently, a canine DMD.<ref><pubmed> 25740330</pubmed> [https://www.ncbi.nlm.nih.gov/pubmed/25740330]</ref>

==Lab 9 Assessment==
'''Group 1 Review'''

You guys have done really well to accumulate a lot of relevant information so far on your wiki page which is definitely a positive for your team. In the context of criterion 1 of the assessment criteria, I am not certain that the key points are clearly described as of yet, there is just a lot of information that is not presented to the reader in a targeted manner, so this definitely needs some work. As I have stated previously the choice of content appears to be adequate to address your topic however you guys need to work on increasing the number of subheadings as well as providing an introduction as the project aims remain unclear. Content is not completely correctly referenced yet, presumably due to the fact that you guys are still making your project page up but referencing is very easy to do correctly on this wiki and I implore you to make sure it is done correctly when it is time to submit the assignment.

As I have alluded to previously, elements of teaching at a peer level were completely missing in this and these definitely need to be addressed, probably by putting entries into your glossary as well as creating a well structured introduction. It would also help if you guys drew some representations of information, such as sketches of pathways. There is certainly evidence of going above and beyond the formal learning activities, which is a major positive for your project. In the context of learning objectives of the course, you guys are addressing the aspect of embryological development but have not addressed the relevance of new technologies in the WnT Pathway.

Overall, there is a lot of potential for you guys to put out a very good wiki page if you clean up your page so that it is more coherent and insert some information that is lacking so that a relatively uneducated reader could understand the WnT signalling pathway from the wiki page. Well done!

'''Group 2 Review'''

At first glance, I was blown away by your team's page. Definitely very impressive and understandable. The key points relating to the Notch signalling process are definitely clearly described however I may recall Dr Hill requesting that teams steer clear of clinical effects of genes(citation needed!). The choice of headings, sub-headings and diagrams show more than a good understanding of the topic area, it may be useful to include a table that summarises the various aspects of the Notch pathway so that readers realise there are different receptors. The content is cited correctly, however, I would not mind reading 'et al' instead of 'and colleagues' more often, I got sick of reading 'and colleagues'.

The information presented is mostly peer friendly in the context of a simple introduction but your glossary certainly needs updating, there are a lot of terms that a lot of students would not understand and a comprehensive checking of your page will offer you a list of words that you need to define. Also lacking are sketches presented in your own hands, instead of reusing published images. There is plenty of evidence that suggests your team has went beyond the formal teaching activities. In the context of the aims of the embryology course, you guys have emphasised the embryonic role of Notch but the aspect of developing technologies appears to have been ignored to an extent.

Overall, you guys have done a very impressive job that only requires minor tweaking, namely slight editing in the context of in text referencing, more comprehensive glossary as well as checking the course aims of embryology to incorporate the second criterion regarding technology. Excellent work!

'''Group 4 Review'''

Nice effort group 4. Key points that relate to the Hedgehog signalling pathway are very succinctly described. Your choice of headings, albeit brief, provides a sense that you guys understand the topic generally but I feel as if you could improve on your subheadings, for example of the Clinical Significances section, I feel as if the diagnosis subheading could be altered. I also feel as if the information in the Organogenesis section could be reworked into an introduction which would allow you to then focus on Organogenesis on its own in more detail. Also, you guys only have one image so far which seems to be slightly lacklustre, you guys definitely need more images. The relevant content is mostly cited correctly, albeit the odd reference located below the marking criteria, I feel as if that is more of a small accident.

The information presented is relatively peer friendly. Perhaps more explanation, for example in the Processing of precursor section as I felt well and truly lost in that area. You guys could do with some hand drawn diagrams or analogies to help explain the information provided. A glossary section would be very helpful in understanding the wiki page, by defining the complex terms such as proteasome(which is misspelt on your page as proteosome). The research that has been done has indicated that you guys have went beyond the formal teaching activities, however, you guys could do more research in the sections that have no information for example 'History', you could even put a timeline in there! In the context of the course aims, he embryological relevance of the Hedgehog pathway is addressed to an extent but as you have missing sections under human disease, there is still work to be done in this section. Also, you should try to complete your current research section to address the second criterion of the course aims regarding new technologies and research.

Overall you guys have had a good start and really just need to start filling in the blanks so to speak. Your team researches information well, just ensure that you fill in your missing sections and think of innovative ways to present information. Nice job!

'''Group 5'''

Your team has a very impressive wiki page, well done! The key points relating to T-Box as well as your choice of subheadings and headings are very good, however I would advise removing 'Good places to look'. In terms of diagrams, tables and graphs, these are present and augment the information presented quite well. The content presented is cited mostly correctly however care must be taken with pictures, which have to be checked for copyright reuse as well as ensuring that they are cited correctly in the first place, I would advise that your team checks each of your pictures to make sure that they are correctly cited.

In the context of peer level education, your content is understandable and written well even though the topic is complex. What is lacking however are using your own explanations as well as interesting hand drawn visual stimuli to present information, this can be easily remedied. Also, completion of the glossary section so that someone can understand complex terms would be useful. With the information that has been provided and the depth of research that has went into the meticulous presentation of information regarding T-box, it is clear that your team has went beyond formal teaching activities, however, perhaps the inclusion of some interactive features on your page such as a video with voice over or a quiz would help augment this criterion. The learning aims of the Embryology course are mostly in line with the information on the wiki page, but there is no section for current research/technologies, which is important to address the second criteria of the course aims.

Overall, you guys did a very nice job that requires only minor touch ups and the addition of a few pieces of information. Don't forget the current research section though, that is pretty important to include in my opinion. Well done!

'''Group 6'''

Good try group 6. Key points appear to be well selected, however perhaps consideration of clinical aspects of your research could be considered useful. Your subheadings should be fixed so that all of your information does not come under the introduction section and also perhaps include more pictures in your project. You guys have a good lay out of information, now you really just need to fill those sections up with information, definitely have a sound understanding of the topic area. There are little to no references as of yet and none of the references in the references section have been cited correctly, this can be fixed by simply using the inbuilt referencing mechanism we have been using for our weekly assessment items. Also, more peer reviewed journal articles should be used and cited to provide authority to your information.

The information presented is very peer friendly and understandable but will need the inclusion of hand drawn diagrams to satisfy this criterion completely. There is not much evidence to suggest that your team has went beyond the formal teaching activities, perhaps incorporate a video or quiz into your work. In terms of the course aims of embryology, you have not satisfied the second criteria regarding new technology/current research as of yet and have vaguely addressed the key criteria regarding TGF and embryological development.

Overall, the areas to be discussed appear to be sound but need to be edited so that the information will flow better. Your team needs to put more information into each section, I would recommend looking at some of the other teams to see how much information is seemingly adequate. Ensure that you reference your information correctly and you should be good when you guys put more research onto your page. Good luck and nice
try!

==New Sub-Heading==
===External Link===
===Internal Link===
https://embryology.med.unsw.edu.au/embryology/index.php/ANAT2341_Lab_1
===References===
[http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=fertilization fertilization]

Talk:2016 Group Project 5

2016-10-07T01:16:46Z

Z5015337:

{{ANAT2341Project2016discussionheader}}
=Peer Review=
===Group 5 Review===

Your team has a very impressive wiki page, well done! The key points relating to T-Box as well as your choice of subheadings and headings are very good, however I would advise removing 'Good places to look'. In terms of diagrams, tables and graphs, these are present and augment the information presented quite well. The content presented is cited mostly correctly however care must be taken with pictures, which have to be checked for copyright reuse as well as ensuring that they are cited correctly in the first place, I would advise that your team checks each of your pictures to make sure that they are correctly cited.

In the context of peer level education, your content is understandable and written well even though the topic is complex. What is lacking however are using your own explanations as well as interesting hand drawn visual stimuli to present information, this can be easily remedied. Also, completion of the glossary section so that someone can understand complex terms would be useful. With the information that has been provided and the depth of research that has went into the meticulous presentation of information regarding T-box, it is clear that your team has went beyond formal teaching activities, however, perhaps the inclusion of some interactive features on your page such as a video with voice over or a quiz would help augment this criterion. The learning aims of the Embryology course are mostly in line with the information on the wiki page, but there is no section for current research/technologies, which is important to address the second criteria of the course aims.

Overall, you guys did a very nice job that requires only minor touch ups and the addition of a few pieces of information. Don't forget the current research section though, that is pretty important to include in my opinion. Well done!

===Group 5 Peer Review===

'''Positive Factors'''

Group 5 have introduced their topic really well, I think it could be improved by putting the second half of their intro under the ‘History’ subheading though and maybe it could be moved up so it is straight after the introduction. The table they have included shows they have considered addressing criteria 4 as I think it makes it easy for students to quickly take in a lot of information. Furthermore, they have addressed criteria 1 and 2 by organising the subheadings and sub-subheadings in a way that gives the page a logical flow. The amount of references already incorporated in their project shows that they have already completed extensive research on the topic area, which addresses criteria 5. Criteria 6 has clearly been addressed in the ‘development’ subsections.

'''Points for Improvement'''

Some improvements that Group 5 could make to their already extensive effort include: changing some of the headings in the table to bold so that they are clearer/easier to read; they could also uncapitalise the subheadings under ‘Abnormalities’ to make the page more uniform; and also formatting the images to incorporate them around the text (rather than breaking up the page each time) would improve the flow of information.

'''Overall'''

Overall Group 5 have already done extensive research as evidenced by the volume of information and various images included in their page, I can see that they have made an effort to address most of the criteria already. The improvements they need to make mainly involve formatting to make the page more student-friendly.
 
 
Group 5: 
 
 

Positive aspects of the project and suggested improvements:
 
 
Upon reviewing this page, it is clear that group 5 has provided numerous headings and subheadings related to Tbx-genes ranging from origins of the genes, their function in embryonic development, abnormalities, history and animal models (criteria 1 and 6). In doing so, the group has also ventured to provide an in-depth explanation of each subheading. Take for example the subheading named, “limb development”, the authors have provided an in-depth description into the role of T-box transcription factors in limb development whilst utilising a diagram to reinforce this description (criteria 2). It also appears that in-text citations have been correctly used to reference the sources of data in most cases (criteria 3). The authors have utilised diagrams and a table to describe various components of the T-box gene ranging from the different types of T-box genes to its mechanisms in embryonic development (criteria 4). The extensive use of diagrams allows the audience to develop a holistic understanding of the various subheadings included, as these diagrams convey the description provided in a visual manner (criteria 5). It is also evident that the group has conducted research into animal models and evolution of the T-box gene, thus demonstrating that the group has investigated areas of research beyond formal teaching activities (criteria 5).
 
 
Improvements which may be made to this page would be to include a timeline regarding the history of the T-box family, as this will display the information in a much more organised and appealing manner. Another improvement which may be made would be to include a YouTube video to introduce the signalling process in development, such as in cardiac and limb development for example. In order to make the wikipage interactive, a further improvement which may be made would be to include a set of multiple choice questions at the end of the page which ask questions about the content covered.
 
 
Negative aspects of the project and suggested improvements:
 
 

Alongside the various positive aspects of this project, there are few negative aspects. A negative aspect identified includes the use of images from Wikipedia pages more than once. It was stated that only one Wikipedia page was allowed to be included as a source. Therefore a suggestion would be to obtain images and data from research articles rather than from Wikipedia pages, as research articles are often a more reliable source of data. It was also noticed that images were not utilised to describe different abnormalities associated with the TBX gene, hence a possible improvement would be to include images depicting such abnormalities. These images may make this section of the page more appealing and engaging to audiences.
 
 

It was also noticed that the image titled “Evolution of the T box gene family”, was incorrectly referenced. Therefore, it is suggested that the authors of the project ensure that the original author of the image are correctly referenced to ensure that copyright laws are not breached. The final negative aspect of the project was that the “Ancient origins and evolution of the T-box gene family” subheading appeared out of place in the page. Therefore a possible improvement would be to include evolution of the T-box gene under the “Origins of the T-box gene” subheading at the beginning of the page as this will create a sense of consistency in the page.
 
 

===Group 5===

First of all, well done on making significant progress on your project! You have addressed all aspects of the pathway involving T-Box genes through subdivision into various headings and subheadings. I particularly liked how there was an inclusion of the specific T-Box gene affected in each of the abnormalities in the subheading itself. The only suggestion I would make is to combine the ‘Ancient origins and evolution of the T-Box gene family’ section with the origins of the ‘T-Box genes’ section to provide a more coherent description of the history of these pathway. You could even form a table to create a timeline of events. In addition, I think it would be beneficial to include the ‘What does T-Box mean?’ as an introduction to the ‘origins of the T-box genes’ section as there is overlap between these sections.

The use of a table to describe the main T-box genes was helpful in providing a brief overview of the components of the pathway and their influence in embryological development. In addition, the link between T-Box genes and embryonic development has been explored considerably. In saying this, greater attention to detail must be paid to explaining abbreviations to aid one’s understanding of the concepts being discussed. For example, what is NKX2-5, Shh and OFT? Though you’ve explained that RA stands for retinoic acid in the ‘Organisms used in animal models for T-Box’ section, this same explanation is not provided in the ‘Limb development’ section where you have discussed that ‘RA and Shh both induced Tbx2’. These small changes will significantly improve the quality of your work.

The inclusion of abnormalities provides great insight into the role of T-Box genes in development. In saying this, though you have explored the effect of the mutation of these genes in animal models, more information is required to explain the effect of these mutations in humans and how they come about. Furthermore, under the heading of ‘Animal models’ there has been discussion mainly of the ‘brachyury gene’ which seems unrelated to animal models due to the lack of a proper introduction. I found the following section (organisms used in animal models for T-Box) to be a better introduction to the topic of animal models. In addition, there has been mention of a number of animal models ‘Drosophila, Xenopus, zebrafish, avians, and mice’ yet only marsupials and amphioxus has been discussed. This could be potentially misleading to readers.

Overall, a fantastic effort has been made. Not only have you touched upon nearly every section of the project, but have included some excellent diagrams and tables which aid understanding of this pathway. In saying this, it is noted that two Wikipedia images have been used though it has been suggested that only one of the images utilised can be from Wikipedia. All information provided was also appropriately referenced and cited. In addition, I think it would be useful to utilise the discussion page to encourage interaction between group members as it allows individuals to provide feedback and suggestions. Hope this helps!

===Group 5 Critical Assessment===
Well done on constructing a thorough Wiki page on the topic of T-box Genes and their Signalling! Viewing the page it is evident numerous headings and subheadings have been provided to accommodate for the large amount of information gathered. Starting off with the introduction I like how you have included a section on what T’-box exactly means, however the information provided in this section talks about the history significantly, hence to turn this into a positive I would suggest adding a table or timeline outlining the major events and discoveries in the past to present this information in a complete, meaningful way. This issue is also seen with the section ‘Origins of the T-box genes’ where major discoveries are highlighted and in which year they occurred. This information can also merge with the history timeline/table.

Within the ‘What does T-box mean?’ section you have also added information on which animal studies were undertaken for the discoveries. To avoid spreading of information and causing confusion for the reader, you could either construct a table to show which animal study was completed in which year, and what discovery it led to as 3 columns, or bring this information down to the section ‘Animal Models’. In saying that, you have attempted to utilize a table and the table works very well with the topic of the different T-box genes, and would prove great help for the viewer.

It is great to see T-box genes and Signalling has been explored further in the field of embryonic development. Extensive information is provided with good use of in- text citations, allowing the reader to navigate to relevant articles. The ability to navigate could be further improved by providing an accessible link to the ‘Abnormalities’ section in a case where you are directing the reader to the section for further information, instead of plain text. Beneath each section for e.g. ‘Limb Development’ Pubmed links have been provided to relevant articles, which is a fantastic idea, however the links have no indication whatsoever of what the article is about. You could add a sentence each next to the links briefly stating what the article is exploring in relation to limb development.

Overall with a few more images, possibly some interactive components such as clips, and a knowledge testing short exam or quiz this Wiki page will stand out. Remember to ensure your information flows well by placing it within appropriate sections!

===Group 5 Peer Assessment===

It is quite clear that what has been provided in your wiki page is extensive and well researched. The inclusion of tables summarizing the different T-box genes although extensive, is very concise and easy to read. I feel that this table really links all the elements of your page together, where you have included its function and related it to embryological development and abnormalities which you go on later to elaborate in other sections. I feel this really complements the introduction and gives a good feel for what’s to come in the rest of the page. The addition of what the term T-box means also is a nice touch, giving context and some history regarding the name.

Your origins section of T-box is quite well outlined, but as mentioned in your page, having a timeline with critical points of discovery with regards to the genes would probably be more beneficial as it would be a lot easier to read a see the time points as a whole. That being said, having the timeline alongside your outline would probably work well, as your outline can serve to elaborate on the timeline. With regards to your subheadings, it seems to they are quite extensive and cover practically all the key components of the T-box genes, and it is also good to see that there is a glossary subheading in place. Content wise there seems to be limited to no issues, but with regards to abbreviations, I have found that the usage hasn’t always been after the fact of providing the full name first. For example, bone morphogenic protein’s abbreviation is used consistently throughout the first part of the wiki page, but it is only described by its full name and then abbreviation later on. This is something you should check out and fix by either adding the full name the first time the abbreviation is used, or adding all these terms to the glossary.

With regards to the pictures they all seem to compliment the sections well and are quite plentiful. That being said though the picture in the “Marsupial forelimb development” does not appear to have the copyright information regarding to its usage, and referencing does not appear to be in full. This is also the same for the picture under the subheading “Organisms used in animal models for T-box”. Other than that the referencing is perfectly fine within the text.

Overall this project is really good and without any major flaws when it comes to the content. A few touch ups here and there with regards to my suggestion above, and your project should be good to go along as the quality is kept at this level.

===Group 5 – T-Box===
First impressions alone it is extremely clear that Group 5 has thoroughly researched this topic have tried hard to include many diagrams and tables to help separate their information up in order to more successfully convey the information across to the reader. Positive aspects of this project include the well-defined subheadings, making the navigation through the page very easy. The introduction is informative and introduces the following subheadings of the project well. The inclusion of what does T-Box mean is also interesting, setting you apart from the other projects. One of the best aspects of the project would have to be the summary table of the main T-box genes, which includes its main expression sites, its function and abnormalities relevant to the specific gene. You have made a note to include a timeline for the history of the T-Box gene, which I think would be successful in summarizing the scientific advances since its discovery, and also help to break up paragraphs of writing. The project appears to be referenced correctly using in-text citations, only query is whether the links to the PMID articles say in the bottom of cardiac and limb development are references or just articles in which you haven’t written on yet and will be referenced appropriately when you do later. The inclusion of a glossary is also a good idea just to help define and explain some of the more difficult terms mentioned.

As for negative aspects of the project, there wasn’t too many. Like for every project, in terms of making it more interactive it might be a good idea to include a YouTube video or animation of the signaling pathway or its role in a specific developmental process, as well as your own hand-drawn image just to fulfill the necessary criteria of this assignment. Furthermore, with some of the smaller images that don’t go the full width of the page, it might be a nice idea to align them to the right as a thumbnail next to their relevant text, so readers see them whilst reading about it. Also remember to make a reference the image you have chosen in your text to emphasise its importance to what you are actually talking about. Although the subheading “good places to look” might just be something for you guys while researching, I think that you could utilize this by including various links with more information on the relevant topics of which you have discussed. This would help to make you page more interactive as well.

This project appears to be extremely well done and is definitely one of the strongest. Most of the criticisms are regarding the formatting of the page and making it more interactive for the reader. All in all this is very well researched project!

===Group 5 Peer Assessment===

Positive aspects of the project and improvements:

Upon reviewing the page, it is evident that there has been a lot of research put in this project. Initially, there is evidence of a range of headings and subheadings which allowed the navigation from one aspect of the project to another extremely easy. This allowed me to confirm that the project is about T-box genes and their signalling. Secondly, it was excellent to see a range of images, tables and graphs as they provided visual aids to learn more about the topic and in general made it easier to accumulate information. Also it was good to see that these tables and images were correctly cited and referenced at the end which meant that there was no breach of copyright laws.

Also, throughout the project there was sufficient amount of information in each subheading which meant that the reader gained all relevant information pertaining to the section that they are reading. It was also great to see a range of abnormalities being added to the project. This meant that you have went above and beyond the scope of the assessment and researched that extra bit to provide additional information about the signalling pathway and complications arising from any mutations. This meant that you successfully satisfied criteria 5 and thus a more rounded project.

Negative aspects of the project and improvements:

This project certainly contains a range of positives but there were minimal negatives that can easily be amended in order to achieve a very high mark. I noticed that there was more than 1 image being used from Wikipedia and the criterion clearly says that a maximum of 1 was allowed. This is not a big deal but just in case there is harsh marking and penalties, it is advised to replace the additional image with another image. In addition, it would be useful to add a glossary of all the terms that one may find confusing such as “homologues”, “heterozygous”, “homology”, “notochord” etc. This in turn will provide the reader with enough information to understand the context of the project and in turn keep them engaged.

Another negative aspect of the project was that the subheading “Ancient origins and evolution of the T-box gene family” randomly appearing nearing the end of the project. This looked a bit out of place and not flowing with the rest of the passage. To correct this it would be advised to add this to the start of the page with the “Origin of the T-box genes” section just so the information clearly flows from one topic to another without creating confusion. Overall, this project is coming along quite nicely. It is evident that a lot of research has been put into constructing a coherent and succinct project but also have the visual cues to back up the main aspects. To maximise marks, it is recommended to reflect on the feedback and correct the minor mistakes.

===Group 5 Peer Assessment===

Positive feedback:

This is a very well, put together and organised page. Everything is very simple and straight-forward make it extremely student friendly and something I would definitely use to learn about T-Box genes.

The introduction along with explanation of the actual meaning of T-box is both informative and also interesting and gives students a good chance to take a break from the heavy load of information and actually indulge in some interesting facts.Following this, the table is one of the most useful things on the entire page and is extremely concise and structurally pleasing. It provides the key and relevant information and allowed me to make connections with T-box genes and their functions straight away.

There is also the use of many pictures throughout the page which definitely aids in visual learning and the more the used the better. The chronological structuring of the page is also very impressive. As I was reading the page I felt like the information that I was gathering was carrying on and helping me understand what was talked about in the next sections.

Critical Assessment:

The chronological structuring although very impressive did fall a little out of place when the sub-headings “Ancient origins and evolution of the T-box gene family” appeared at the end of the page when it seems like this is something that should be included in the start. It would be thoroughly recommended to utilised hand drawings to explain some of the concepts, especially when introducing the signalling because this would really compliment your already easy to understand introductions and really enhance learning/understanding.

Lastly I think it would be a good addition to your project to include some information on the current research that is being conducted on t-box genes and also if there are treatments for the abnormalities. This page is looking amazing so far so keep up the good work!

Some searches to get us started:
[http://www.ncbi.nlm.nih.gov/sites/gquery?term=t-box ''T-box'']
[http://www.ncbi.nlm.nih.gov/sites/gquery?term=tbx ''tbx'']

[[User:Z5020373|Z5020373]] ([[User talk:Z5020373|talk]]) 14:44, 26 August 2016 (AEST)
PMID 25294936 - a relatively recent article that provides background info on the T-box gene family
PMID 16285859

[[User:Z3516832|Z3516832]] ([[User talk:Z3516832|talk]]) 14:52, 26 August 2016 (AEST)
http://www.columbia.edu/itc/hs/medical/humandev/2007/HD15/HD15.pdf

[[User:Z5020373|Z5020373]] ([[User talk:Z5020373|talk]]) 11:32, 16 September 2016 (AEST) Does anyone know how to draw up a table on the page? Thanks.

User:Z5015337

2016-10-07T01:15:36Z

Z5015337:

{{ANAT2341Student2016}}
==Lab 1 Assessment==
<pubmed>26446757</pubmed>

In the aforementioned research article, the "Onobrychis Viciifolia" or rather, sanfoin is explored in detail with respect to its ability to self fertilise and therefore be a sustainable and useful plant for its local ecosystem. This is due to its ability to reduce the need of nitrogen fixation by bacteria as a Legume. On top of this, Sanfoin has tannins in it that assist with the break down of proteins and as such, it is beneficial to animals.

This research article utilises naturally directed pollination and artificially directed pollination to compare rates of self fertilisation. Interestingly, the plants of sanfoin that used artificially directed pollination had much higher rates of self fertilisation than the natural counterpart. Whilst there are other results obtained, these are the main results that by implication indicate that we can assist the growth of local plant systems by artifically pollinating sanfoin, which will provide nutrients and reduce the dependence on nitrogen fixation for plants to obtain nitrogen.

{| width=95%
|-bgcolor="FAF5FF"
| [mailto:m.hill@unsw.edu.au Mark Hill] 18 August 2016 - You have added the citation correctly and written a good brief summary of the article findings. However, a plant study on "fertilisation" is not really what I was asking, in particular as this is not a Botany course, please try and focus on course content.

| width=100px| Assessment 4/5
|}
==Lab 2 Assessment==
[[User:Z8600021|Mark Hill]] ([[User talk:Z8600021|talk]]) 10:17, 19 August 2016 (AEST) you need to use the full file name (.jpeg).

[[File:Extracellular calcium levels compared to Spermatozoa levels.jpeg]]

Effect of extracellular Ca2+ depletion on the human zona pellucida-induced intracellular [Ca2+] increase in spermatozoa<ref><pubmed>PMC1712232</pubmed>
[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1712232/]</ref>

{| width=95%
|-bgcolor="FAF5FF"
| [mailto:m.hill@unsw.edu.au Mark Hill] 29 August 2016 - All information Reference, Copyright and Student Image template not included with the file and citation not referenced on your page here. I cannot complete the assessment without knowing the original source (reference for this image). Please update so that I can complete the assessment.

| Assessment ??
|}
===Lab 3 Assessment===
{| width=95%
|-bgcolor="FAF5FF"
| [mailto:m.hill@unsw.edu.au Mark Hill] 29 August 2016 - Quiz Mesoderm and Neural

| Assessment 5/5
|}

===Lab 4 Assessment===
====Gastrointestinal Tract Developmen====
.

<quiz display=simple>

{The mesoderm consists of epithelium, connective tissues, blood vessels, mesentry, smooth muscle.
| type="()"}
-   true
+   false
|| Whilst the mesoderm consists of connective tissues, blood vessels, mesentry and smooth muscle, epithelium is located in the endoderm and not the mesoderm .





{Select the most correct option of the following options:
|type="()"}
-   The superior mesenteric artery supplies the hindgut
-   The foregut is suppled by the inferior mesenteric artery
-   The celiac artery supplies the midgut
+   The superior mesenteric artery supplies the midgut
||The superior mesenteric artery supplies the midgut, the celiac artery supplies the foregut and the inferior mesenteric artery supplies the hindgut.



{Which of the following statements about lumen abnormalities are correct:
|type="[]"}
-   Atresia is a term that refers to the narrowing of the lumen
+   The formation of parallel lumens is a form of stenosis
+   An abnormality that results in interruption of the lumen is Atresia
-   Duplication results in perpendicular lumen
|| The key to solving these sorts of questions are to ensure that the questions are read carefully as there is usually a trick in the wording. Atresia refers to an interruption of the lumen, not narrowing of the lumen. Parallel lumen formation is a form of specialized stenosis. As mentioned prior, Atresia refers to an interruption of the lumen. Duplication will result in the formation of parallel lumens and not perpendicular lumens.

{Select the most correct option of the following options in the context of patterning signals:
|type="()"}
-   Endothelin is expressed in the anterior part of the primitive gut.
-   Cdx2 regulates the migration of enteric neural tube cells
+   GDNF regulates the migration of enteric neural crest cells
-   Sox2 is expressed in the posterior part of the primitive gut.

||Endothelin regulates the migration of enteric neural crest cells/ Cdx2 regulates the migration of enteric neural CREST cells, not tube. GDNF regulates the migration of enteric neural crest cells. Sox2 is expressed in the ANTERIOR part of the primitive gut.

</quiz>

==Lab 5 Assessment==
I have completed the prescribed questionnaire during lab.

==Lab 6 Assessment==
1. A known genetic mutation that is associated with cleft lip is the mutation of the p63 or TP63 which allows the encoding of the Tumour protein p63.

2. A research article that explores this gene is:

<pubmed>2564545</pubmed>

3. Mutations of the p63 gene are detrimental as it is a critical regulator that prevents a host of defects in development, such as ectodermal dysplasia. Without the presence of this gene in mice, the mice died at birth and had truncated limbs as well as epidermal defects<ref><pubmed>16524929</pubmed>[http://www.ncbi.nlm.nih.gov/pubmed/16524929]</ref>.

In the context of cleft palate syndrome and the p63 gene, there is not a clear reason as to why mutations of the p63 gene can result in cleft palate but as cleft palate is a form of ectodermal dysplasia and functioning p63 prevents dysplasia, a connection can be made <ref>[https://ghr.nlm.nih.gov/gene/TP63#conditions]</ref>.
==Lab Attendance==
[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]]) 9/09

[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]])23/09[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]])

==Lab 7 Assessment==
1. The dystrophin gene is located on the locus of the X chromosome and is responsible for the transcription of dystrophin. A mutation of this gene will therefore result in altered expression of the muscle isoform, dystrophin<ref><pubmed>14636778</pubmed></ref> . Mutations like these can result in Autosomal recessive muscular dystrophy and Duchenne and Becker muscular dystrophies to name a few.

2. Dystrophin is a critical protein that is responsible for linking the actin filaments to the sarcolemma, which is a protein that is located in the interior of the plasma membrane of individual muscle fibres<ref><pubmed>11917091</pubmed></ref>. Dystrophin is critical in ensuring the stability of muscle fibres and without it intracellular calcium handling is altered resulting in muscular function being impaired<ref><pubmed>15470384 </pubmed></ref>.

3. Other organs that are affected by this disorder are the heart and those responsible for respiration as there is gradual loss of healthy muscular fibres which by cellular repair mechanisms are replaced with inelastic fibrous tissue resulting in less effective contractions resulting in cardiac and respiratory failure<ref><pubmed>4767260</pubmed></ref> .

4.

5 The animal models available for muscular dystrophy are historically the MDX mouse and more recently, a canine DMD.<ref><pubmed> 25740330</pubmed> [https://www.ncbi.nlm.nih.gov/pubmed/25740330]</ref>

==Lab 9 Assessment==
'''Group 1 Review'''

You guys have done really well to accumulate a lot of relevant information so far on your wiki page which is definitely a positive for your team. In the context of criterion 1 of the assessment criteria, I am not certain that the key points are clearly described as of yet, there is just a lot of information that is not presented to the reader in a targeted manner, so this definitely needs some work. As I have stated previously the choice of content appears to be adequate to address your topic however you guys need to work on increasing the number of subheadings as well as providing an introduction as the project aims remain unclear. Content is not completely correctly referenced yet, presumably due to the fact that you guys are still making your project page up but referencing is very easy to do correctly on this wiki and I implore you to make sure it is done correctly when it is time to submit the assignment.

As I have alluded to previously, elements of teaching at a peer level were completely missing in this and these definitely need to be addressed, probably by putting entries into your glossary as well as creating a well structured introduction. It would also help if you guys drew some representations of information, such as sketches of pathways. There is certainly evidence of going above and beyond the formal learning activities, which is a major positive for your project. In the context of learning objectives of the course, you guys are addressing the aspect of embryological development but have not addressed the relevance of new technologies in the WnT Pathway.

Overall, there is a lot of potential for you guys to put out a very good wiki page if you clean up your page so that it is more coherent and insert some information that is lacking so that a relatively uneducated reader could understand the WnT signalling pathway from the wiki page. Well done!

'''Group 2 Review'''

At first glance, I was blown away by your team's page. Definitely very impressive and understandable. The key points relating to the Notch signalling process are definitely clearly described however I may recall Dr Hill requesting that teams steer clear of clinical effects of genes(citation needed!). The choice of headings, sub-headings and diagrams show more than a good understanding of the topic area, it may be useful to include a table that summarises the various aspects of the Notch pathway so that readers realise there are different receptors. The content is cited correctly, however, I would not mind reading 'et al' instead of 'and colleagues' more often, I got sick of reading 'and colleagues'.

The information presented is mostly peer friendly in the context of a simple introduction but your glossary certainly needs updating, there are a lot of terms that a lot of students would not understand and a comprehensive checking of your page will offer you a list of words that you need to define. Also lacking are sketches presented in your own hands, instead of reusing published images. There is plenty of evidence that suggests your team has went beyond the formal teaching activities. In the context of the aims of the embryology course, you guys have emphasised the embryonic role of Notch but the aspect of developing technologies appears to have been ignored to an extent.

Overall, you guys have done a very impressive job that only requires minor tweaking, namely slight editing in the context of in text referencing, more comprehensive glossary as well as checking the course aims of embryology to incorporate the second criterion regarding technology. Excellent work!

'''Group 4 Review'''

Nice effort group 4. Key points that relate to the Hedgehog signalling pathway are very succinctly described. Your choice of headings, albeit brief, provides a sense that you guys understand the topic generally but I feel as if you could improve on your subheadings, for example of the Clinical Significances section, I feel as if the diagnosis subheading could be altered. I also feel as if the information in the Organogenesis section could be reworked into an introduction which would allow you to then focus on Organogenesis on its own in more detail. Also, you guys only have one image so far which seems to be slightly lacklustre, you guys definitely need more images. The relevant content is mostly cited correctly, albeit the odd reference located below the marking criteria, I feel as if that is more of a small accident.

The information presented is relatively peer friendly. Perhaps more explanation, for example in the Processing of precursor section as I felt well and truly lost in that area. You guys could do with some hand drawn diagrams or analogies to help explain the information provided. A glossary section would be very helpful in understanding the wiki page, by defining the complex terms such as proteasome(which is misspelt on your page as proteosome). The research that has been done has indicated that you guys have went beyond the formal teaching activities, however, you guys could do more research in the sections that have no information for example 'History', you could even put a timeline in there! In the context of the course aims, he embryological relevance of the Hedgehog pathway is addressed to an extent but as you have missing sections under human disease, there is still work to be done in this section. Also, you should try to complete your current research section to address the second criterion of the course aims regarding new technologies and research.

Overall you guys have had a good start and really just need to start filling in the blanks so to speak. Your team researches information well, just ensure that you fill in your missing sections and think of innovative ways to present information. Nice job!

'''Group 5'''
Your team has a very impressive wiki page, well done! The key points relating to T-Box as well as your choice of subheadings and headings are very good, however I would advise removing 'Good places to look'. In terms of diagrams, tables and graphs, these are present and augment the information presented quite well. The content presented is cited mostly correctly however care must be taken with pictures, which have to be checked for copyright reuse as well as ensuring that they are cited correctly in the first place, I would advise that your team checks each of your pictures to make sure that they are correctly cited.

In he context of peer level education, your content is understandable and written well even though the topic is complex. What is lacking however are using your own explanations as well as interesting hand drawn visual stimuli to present information, this can be easily remedied. Also, completion of the glossary section so that someone can understand complex terms would be useful. With the information that has been provided and the depth of research that has went into the meticulous presentation of information regarding T-box, it is clear that your team has went beyond formal teaching activities, however, perhaps the inclusion of some interactive features on your page such as a video with voice over or a quiz would help augment this criterion. The learning aims of the Embryology course are mostly in line with the information on the wiki page, but there is no section for current research/technologies, which is important to address the second criteria of the course aims.

Overall, you guys did a very nice job that requires only minor touch ups and the addition of a few pieces of information. Don't forget the current research section though, that is pretty important to include in my opinion. Well done!

==New Sub-Heading==
===External Link===
===Internal Link===
https://embryology.med.unsw.edu.au/embryology/index.php/ANAT2341_Lab_1
===References===
[http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=fertilization fertilization]

Talk:2016 Group Project 4

2016-10-07T00:47:58Z

Z5015337:

{{ANAT2341Project2016discussionheader}}

=Peer review=

===Group 4 Review===

Nice effort group 4. Key points that relate to the Hedgehog signalling pathway are very succinctly described. Your choice of headings, albeit brief, provides a sense that you guys understand the topic generally but I feel as if you could improve on your subheadings, for example of the Clinical Significances section, I feel as if the diagnosis subheading could be altered. I also feel as if the information in the Organogenesis section could be reworked into an introduction which would allow you to then focus on Organogenesis on its own in more detail. Also, you guys only have one image so far which seems to be slightly lacklustre, you guys definitely need more images. The relevant content is mostly cited correctly, albeit the odd reference located below the marking criteria, I feel as if that is more of a small accident.

The information presented is relatively peer friendly. Perhaps more explanation, for example in the Processing of precursor section as I felt well and truly lost in that area. You guys could do with some hand drawn diagrams or analogies to help explain the information provided. A glossary section would be very helpful in understanding the wiki page, by defining the complex terms such as proteasome(which is misspelt on your page as proteosome). The research that has been done has indicated that you guys have went beyond the formal teaching activities, however, you guys could do more research in the sections that have no information for example 'History', you could even put a timeline in there! In the context of the course aims, he embryological relevance of the Hedgehog pathway is addressed to an extent but as you have missing sections under human disease, there is still work to be done in this section. Also, you should try to complete your current research section to address the second criterion of the course aims regarding new technologies and research.

Overall you guys have had a good start and really just need to start filling in the blanks so to speak. Your team researches information well, just ensure that you fill in your missing sections and think of innovative ways to present information. Nice job!

===Group 4 Peer Review===

'''Positive Factors'''

Group 4 have provided well-written information that I found was easy to follow despite not having an extensive understanding of the topic (covering criteria 1). Another positive aspect of this Group’s effort is the integration of the references, which makes it easy for students to access the resources they have used; already it seems that they have done extensive research on the topic (covering criteria 5). From looking at the subheadings it appears that the scope of the topic will be covered well (which will address criteria 2). Furthermore, the image at the top of the page provides a great visual to aid students’ understanding of and engagement in the topic (showing they have begun to address criteria 4). They have also directly related subsections to embryology, which covers criteria 6.

'''Points for Improvement'''

Some aspects of Group 4’s page that would improve their project include: the image at the top of the page could be better if a title and short explanatory caption accompanied it on the page; use of more diagrams throughout the page would also better address criteria 4; and under the ‘Animal Models’ heading, maybe shortening all the sub headings just to the animal name would make it a little more succinct and clear.

'''Overall'''

Overall this page has shown efforts at addressing a few of the assessment criteria, however still needs some improvements to make the page more suitable to engaging and informing students.
 
 
Group 4:
 
 
Positive aspects of the project and suggested improvements:
 
 

Group 4 has provided numerous headings related to the Hedgehog pathway, such as its involvement in organ development, neural development as well as its mechanism of signalling during embryonic development (criteria 1). The group has also used an image of the signalling pathway to help provide a visual description of the different components of Hedgehog signalling (criteria 2). The authors of this project have also provided in-text citations for all information utilised and have also included a list of references at the end of their page (criteria 3). It is also evident that the group has investigated the involvement of the Shh signalling pathway outside of the scope of human embryonic development by exploring its role in mice, chicks and fruit flies, which is excellent (criteria 5 and 6). The authors have also began to include new research and abnormalities related to the Shh pathway (criteria 1).
 
 

In order to further improve these positive aspects, the authors may provide a written description of the signalling pathway alongside the diagram utilised. This is because it is difficult to understand the signalling pathway just by looking at a diagram. Also, a suggestion would be to include a greater variety of diagrams and tables to support the descriptions already provided. Diagrams may relate to the animal models or the abnormalities described. A table may be utilised to summarise the history of the signalling pathway, such as different components of the pathway that were discovered and the year in which they were discovered. Additionally, whilst it appears that most of the information is correctly referenced, the authors have not correctly referenced the diagram that has been utilised to describe the signalling pathway, which is a breach of copyright laws. Therefore, a suggestion would be to ensure that all diagrams are referenced when added to the page.
 
 

Negative aspects of the project and suggested improvements: 
 
 

Whilst there were positive aspects to this project, a key negative aspect of the project is that the authors have not provided an introduction describing what the Hedgehog signalling pathway is. The introduction may include an overview of the nature and role of the hedgehog signalling pathway in embryonic development, thereby introducing headings in your page. It is also evident that the authors have not met criteria 2 completely, in that a small number of subheadings were utilised. Take for example the heading, “organogenesis”, no subheadings have been created under this heading. A suggested improvement would be to include subheadings relating to specific organs formed by the actions of the Shh pathway, accompanied by an in-depth description and diagrams. It is also evident that the authors utilise complex terminology within their description that often make it difficult to grasp certain concepts. Terms include “knockout”, “autocrine”, “appendage” and “paracrine” for example. A suggestion for improvement would be to include a table of glossary terms at the end of the page, defining these terms.
 
 
It also appears that the authors have not provided a history regarding the Hedgehog signalling pathway and its discovery. A suggestion would be to include a timeline regarding the discovery of this signalling pathway, as it provides the audience with a background of how Shh came to be known.
 
 

===Group 4===

A good start has been made to the project with the appropriate selection of headings and subheadings which provide a brief overview of what is to be discussed in terms of the Hedgehog signalling pathway. By breaking down the mechanism of the pathway, it made the foreign concept much easier to understand. In saying this, this section is quite text-heavy and may benefit with the relocation of the included diagram or even inclusion of other diagrams and flowcharts to engage readers. With the introduction of a fairly new concept, the inclusion of visual or audio stimuli and maybe even a short quiz may encourage interaction with readers.

The discussion of this pathway in mammals exposed readers to the diversity of the Hh signalling pathway but in saying this, the inclusion of a table may be useful to compare and contrast the differences between the pathways in mammals and insects. Overall, this section was well written. On the other hand, when considering the section on animal models, it provided insight into the role of Hh signalling pathway on embryological development and offered a brief introduction to the abnormalities caused by disruptions of this pathway. Once again, the inclusion of diagrams would be useful in this section to provide visual insight into the research being performed.

Though there has been significant exploration of the mechanism and animal models utilised in this pathway, more work is needed to link this pathway to embryological development and this could provide a good leeway into understanding the abnormalities associated with disruption of this pathway. This project can be significantly improved simply by focusing on making it more interactive ad engaging with the inclusion of a variety of stimuli like tables, diagrams, quizzes and even videos. In addition, all information has been well cited and referenced and there has been substantial communication between group members, allowing team members to provide feedback and suggestions thus, ultimately increasing the quality of the work produced.

===Group 4 – Hedgehog Pathway ===
Positive aspects of this project include that Group 4 appear to have well defined subheadings, which function well to help the reader navigate through the page. The information is appropriately referenced using in-text citations, appearing to be from both primary and review articles. There is a significant amount of research on the mechanisms of the pathway but less of a focus on the role of this pathway in embryonic development, which I think is really important in order to relate it back to what we are leaning in both the lectures and tutorials. I think the inclusion of current research is a very important aspect to include in this project, as it identifies the current direction in which this research is heading. This might be also interesting to link to its clinical significance and abnormalities in the signaling pathway.

However, some negative aspects of the page include the lack of an introduction as this essentially establishes your page. You need to include a brief outline of the signaling pathway, a summary of its role in development and the other aspects of it you are looking to discuss. Furthermore, the inclusion of an image outlining the signaling pathway without any information inducing or explaining it should be corrected. The project appears to be very informative but isn’t very interactive and lacks images. Perhaps sourcing images of results from some of the primary articles, which you have referenced or include videos outlining the signaling pathway, might be a useful addition. It might be a good idea to include a glossary at the bottom of the page to help readers to better understand some of these more difficult terms. Also under the subheading of history, like in some of the other projects, a table could be a useful addition, just summarizing all the scientific advances regarding this pathway since it was first discovered, this helps set up how far we have come and then may be helpful when talking about the direction in which we are heading under current research.

In conclusion, this looks like it’s on its way to being a successful project. In summary though, a greater emphasis on its role in embryonic development and conscious effort to make the page more interactive and engaging for the reader will go a long way.

===Group 4 Peer Assessment===

Positive aspects of the project and improvements:

At initial glance I can see a range of headings and subheadings which just made it easier to navigate from one aspect of the project to another. This satisfied the requirements for criteria 1 and 2. This also allowed me to recognise the main topic of the project is the Hedgehog signalling pathway. There is also an addition of an image of the pathway which was great to see as it outlines the main components of the pathway and in general educates the reader about the signalling pathway. This provided a visual stimulus/ description which in turn engaged the reader to find out more about the topic.

It was also good to see correct in text citations and a references list at the end which in turn satisfied criteria 3. To satisfy criteria 5 it was excellent to see information that was well beyond the required information. An example of this is when discussing the role of the pathway in not only humans but also in mice, chicks and fruit flies. The group also began to include new research and abnormalities related to the Shh pathway which aided in rounding off criteria 1.

In order to improve the already positives of this project it would be advised to add a description to the image just so the reader can have some sort of summary about the main points of the image/ pathway. Also, addition of diagrams or tables in some of the subheadings would be good as it will keep the reader interested and in general provide a visual aid. Also it is necessary to cite and provide a reference of the image as it breaches the copyright laws.

Negative aspects of the project and improvements:

Although there are positives to the project, there are a few negatives that can easily be fixed. It is crucial to put in an “Introduction” heading and providing relevant information. This in turn will create a coherent project as it flows from one aspect to another whilst simultaneously providing a brief overview of the Sonic Hedgehog Pathway. Although you have explored the mechanism in animal models it is imperative to link this to embryological development. Also, addition of diagrams, interactive quizzes and tables is necessary to satisfy criteria 3, since 1 image is not enough.

Adding a glossary of terms at the end of the project is needed to clarify any words or phrases that have not been previously encountered such as “organogenesis”, “paracrine”, “dephosphorylation” etc. Overall, the project is coming along nicely and with the recommended amendments, a high mark is definitely in order.

===Group 4 Peer Assessment===

Positive Assessment:

I am very impressed with the level and depth of information provided in this page so far. It is quite evident that you guys have gone to great effort and lengths to research and find relevant information regarding hedgehog signalling. The research conducted is also further solidified with the correct use of citations which link the information with their articles and allow the user to learn more if required. There is almost 34 references already provided which is a testament to the work that has been put in by the group. Well done!

I love the very detailed explanation of animal models used to investigate hedgehog signalling and there is an abundance of information provided for this where as I’ve noticed other groups tend to very lightly touch this topic.

Critical Assessment:

The page is looking very good so far but in my opinion there are a few ways in which it can be improved.

Although the information is in-depth and thorough it can be a little intense at times. I would recommend using more dot points or look into using tables to categorise information into a more user friendly structure. This can also be achieved by using more subheadings to further dissect the information and make it less imposing when reading as this content can be difficult to understand at first. I would also have a nice and clear introduction at the beginning of your page as it essential for the students entering your page to be able to familiarise themselves with Hedgehog signalling before diving into the more complicated information.

I would also make better use of the subheadings, so that they reflect more of the marking criteria in particular hedgehog signalling role in embryology. I didn’t see too much content outlining and explaining this and this is a major part of the project. It would also be a good idea to draw a picture rather than using one to explain the mechanism as simplified visual aids always help. Lastly, try including a glossary as there were many terms that I was very unfamiliar with, such as organogenesis.

===Peer Assessment: Project 4: Hedgehog signalling pathway===
====1. The key points relating to the topic are clearly described. ====
The key points related to the topic are clearly described however the introduction is a little limited , as there is no information just a figure without any text related to the figure.

====2.The choice of content, headings and sub-headings, diagrams, tables, graphs show a good understanding of the topic area. ====
This wiki does seem to have a very extensive list of contents, which demonstrate that the topic is divided into clear interesting sections. However it is not finished and there are empty headings with no text underneath. There is only one figure but there is no text related to these figures so it makes it hard for the reader to know what this means. There are no tables and no other illustrative diagrams. This wiki would benefit a great deal with more figures, table and perhaps a you tube video.

====3. Content correctly cited. ====
Yes it seems the content is cited correctly. There is an extensive list of references. However there is some information that is not cited at all e.g. under Organogenesis. This needs to be cited.

====4. The wiki has an element of teaching at a peer level using the student's own innovative diagrams, tables or figures and/or using interesting examples or explanations. ====
There are no graphs, or tables and one figure that is floating in the introduction and start of the topic. Clearly this can be improved. The wiki does use examples with Drosophilia and Mammals which is great and interesting.

====5. Evidence of significant research relating to basic and applied sciences that goes beyond the formal teaching activities. ====
This is evident that the students have done a lot of research in this topic and are innovative with their examples using Drosophilia and Mammalia however there is still headings without content that needs to be filled.

====6. Relates the topic and content of the Wiki entry to learning aims of embryology. ====
There is a heading on neural development but no text and some information on organogenesis which does correspond to learning aims in Embryology. However more information is clearly needed.

====7. Clearly reflects on editing/feedback from group peers and articulates how the Wiki could be improved (or not) based on peer comments/feedback. Demonstrates an ability to review own work when criticised in an open edited wiki format. Reflects on what was learned from the process of editing a peer's wiki. ====
There seems to be editing in this Wiki however the students need to come together to talk about what is missing: i.e. introduction is missing.

====8. Evaluates own performance and that of group peers to give a rounded summary of this wiki process in terms of group effort and achievement. ====
This is hard to tell. There seems to be an overall group effort but some sections have missing content and it either seems one student is not pulling weight or that section will be a group effort and the group has not worked on it yet.

====9. The content of the wiki should demonstrate to the reader that your group has researched adequately on this topic and covered the key areas necessary to inform your peers in their learning. ====
Yes so far there is adequate research, a lot of references cited but some key sections are empty. It seems that the group has used the Discussion section to communicate between each other.

====10. Develops and edits the wiki entries in accordance with the above guidelines. ====
Yes this group has edited the wiki using the guidelines.

[[User:Z5019880|Z5019880]] ([[User talk:Z5019880|talk]]) 14:58, 26 August 2016 (AEST) Hey guys, I have added some sub-headings for the hedgehog signalling pathway, feel free to add any headings that might be useful for the topic, or suggest a different topic.

Hey guys, I've started doing some research on the animal models for the Hedgehog signalling pathway. I'm currently finding it a little difficult understanding some of the terms when researching the experiments done on Drosophila melanogaster so I was wondering if you had any suggestions as to how much detail to include. Also I have included some links that maybe useful for those researching mechanism and history:
<ref><pubmed>17925578</pubmed></ref>
<ref><pubmed>26839340</pubmed></ref>

Also, I thought I would just put in writing here that we want everyone to have completed their parts by the end of mid semester break so that we can meet up the following week to fix any issues with formatting and work on the introduction, conclusion etc. Thanks guys!!
P.S. Did Mark mention that we shouldn't use research articles?

[[User:Z5019880|Z5019880]] ([[User talk:Z5019880|talk]]) 23:30, 12 September 2016 (AEST) Hey, what you have added is really good! To be honest I'm not completely sure about how technical we have to be, because I have also found my self that there is a lot of chemistry when it comes to the signalling pathways etc. which makes it incredibly difficult for me to understand. At this point I reckon what you have now is enough, but we can always revisit it when we have added more to the page, to keep the content at a consistent depth. Also with regards to the research articles, I'm not entirely sure what Mark said, but I'm sure it would be alright to see what is written, and click into the citations to get further information, and just cite that. Anyway I've added a small piece on the processing of the Hh protein, but am unsure if It would be necessary to go more into the chemistry behind how the auto-cleavage occurs.

So I've read what you have written and I think it sounds coherent and it's also very easy to understand so good job! I think I'll do a little more research, I think it might be a little tedious to add information of Shh knockout mice considering the experiments on the chick embryo were quite similar but I'm open to suggestions. I was also thinking it would be useful to include a link to a short youtube video of some sort that would be able to visually explain the Hh signalling pathway (something like this https://www.youtube.com/watch?v=w1xXD9kss2w but unfortunately this video has no audio but has some good visual and written cues). In regards to an image, I actually found a pretty decent image of this pathway but I'm not too sure if we can use it due to copyright. It says we can if it's not for commercial use so I think we should be ok.

Please let me know what you think of the diagram. I've just added something that looks like it could be helpful but feel free to edit/remove it if you don't think it is appropriate :)

[[User:Z5019880|Z5019880]] ([[User talk:Z5019880|talk]]) 22:28, 26 September 2016 (AEST) The diagram looks great! I reckon as long as we include all the copyright it should be fine. We can probably eventually move the image next to the mechanism of signalling section when it is finished. I have started it, and will continue finishing it tomorrow, so if there are any issues with how I'm going about it, please don't hesitate to tell me.

Good idea! I've added some information on Shh Knockout mice so any feedback on what I have written will be greatly appreciated! I'm also thinking of looking into videos that we could link as part of our assignment to make the concept easier to understand.

[[User:Z5019880|Z5019880]] ([[User talk:Z5019880|talk]]) 21:30, 28 September 2016 (AEST) Hey, I've read your section on Shh and it seems good. In terms of what you could add, do you reckon it is appropriate to talk about the advantage of using each of the models over one another, and possible problems you might encounter with each model. I get that it's probably hard to find material on that, so don't worry if that's the case. Also a video would be a great idea, although we should first check with Mark with regards to what sources would be appropriate. Anyway I have finished the first part of the mechanism part regarding the general pathway for Hh proteins that have specifically been studied in the fruit fly, and will continue onto vertebrates later. I was wondering from what you guys have studied on this pathway if I have covered most of the areas sufficiently and in a coherent matter. Any other feedback is also appreciated.

I've read what you've written and you've successfully made it really easy to understand. From the knowledge I've gained through reading articles on this pathway, I don't think you have missed anything thus far. The only improvement I could suggest is maybe referencing an image in your explanation so that readers have a visual stimulus to refer to to ease understanding of the pathway. In regards to looking at the differences between the models, I genuinely tried to find a comparison between the animal models but was met with no such information unfortunately. I'll try and have a look sometime soon. Also, I was thinking maybe we could include a quiz of some sort to make our project more interactive. We could do this by adding a quiz after each section or just one quiz at the very end. Our project is also quite text heavy so I think we should find more images and other stimuli to make it more interesting. We should create a timeline of events for the history of the pathway in the form of a table. Also, should we create a glossary?

Also, quick question, who's handling history, function and current research?

=== Group 4===
This web page is developing well, but has many areas that need completion. Starting the web page with the flowchart of the hedgehog signalling pathway is not recommended, as the reader has not been introduced to the topic at all and does not know what any of the terms and abbreviations mean. This image would serve better further down in the web page where the reader has knowledge of this signalling process and what is involved to then apply and consolidate in the image. More images can also be included in this web page, such as an image of a hedgehog at the top of the page, which would be an interesting and humorous way to grab the reader’s attention, which is required to fulfil the criteria for this assessment. Images in the animal model section would also enhance the reader’s understanding.

Many subheadings have been included, but could be improved on their clarity. For example, the heading “Mechanism” is not very specific and thus could be improved to identify which mechanisms are being spoken about. A “History” subheading has also been included with no information. A timeline of the history of research associated with the hedgehog signalling pathway would be very comprehensive, including where future research is headed. This research should include why there are question marks (“?”) in yellow in the diagram at the top of the web page, as these could be areas where future research is heading. Ensure this table/timeline is well referenced, including names of researchers for depth of information. A glossary section should also be included to enable to reader to keep track of the different terms and abbreviations used in this web page. Terms in this list could include information on the abbreviations in the diagram included: Cos2, PKA, Slimb and a range of other terms.

A “Human disease” heading has also been included. No information has been added to this section as more research by the group members must be carried out. This heading could be more specific, such as titling it as “abnormalities” as “Human disease” can be in reference to a wide range of issues, whereas “abnormalities” or something similar is more topic specific. Images of the effects of these abnormalities would also be an interesting addition, including treatments for the diseases and their symptoms as well as future research areas. The “Animal Models” section contains substantial textual information. Images would enhance this section, such as images of the animals being studied and short videos of their embryological development. A greater focus on human embryology is needed throughout the entire web page as there is a substantial amount of information on the hedgehog signalling pathway in animals.

In text referencing has been carried out throughout the web page which is commended, and an extensive reference list is developing well. Be sure to reference information twice (using the same reference number) when they are being mentioned, so that the reader has a direct link to where this is being sourced from. For example, another reference for when “Chiang et al., 2001” is mentioned would be appropriate, as the preceding paragraph referenced this work without specifically mentioning Chiang. More in-text referencing in the “Blockage of Shh Signalling in Forebrain Neuroectoderm of Chick Embryos” section would also be appropriate, even if the same references are being re-used. This would make it easier for the readers of the web page to easily access further information at any point in the web page.

User:Z5015337

2016-10-07T00:47:34Z

Z5015337:

Talk:2016 Group Project 2

2016-10-06T23:59:20Z

Z5015337:

{{ANAT2341Project2016discussionheader}}
=Peer Review=
 
 
Group 2:
 
 
Positive aspects of the project and suggested improvements: 
Group 2 has provided a variety of different topics related to the Notch receptor, such as its molecular pathway, its role in embryonic developing both in humans and animals as well as abnormalities caused by disruption in the receptor’s normal function (criteria 6). This variety is excellent, as it informs the audience of various aspects of the Notch receptor ranging from normal to abnormal development as well as newly emerging research (criteria 1.). Group 2 has also utilised both tables and diagrams to represent Notch receptor’s history and signalling pathway respectively (criteria 2). The use of diagrams is a great idea as it allows peers to understand the complexity of the signalling pathway in a much simpler manner (criteria 4).
 
 
In addition, the authors have correctly utilised in text citations when referencing all sources and have created a list of references at the conclusion of the page (criteria 3). Group 2 also investigated specific components of organ development which was another magnificent feature of their page, such that they divided cardiovascular development into different stages including “heart valve development” and “trabeculation” for example. This allows for an in-depth understanding of organ development with respect to the Notch receptor, rather than a general overview of the receptor’s involvement (criteria 5 and 6). The authors also have extended beyond Notch’s involvement in human embryonic development by exploring its role in animal embryonic development (criteria 5).
 
 
Although there are many positives, a possible improvement to this outstanding wiki would be to include a table of the different types of Notch receptors that exist and their different roles in embryonic development. This will allow the audience to understand that there is not just a single receptor playing a role in embryonic development but multiple. Another suggestion would be to add more subheadings under the “Central nervous system” development, as this subheading appears to have a lot less information compared to others. Also, it is obvious that there are different pathways for this receptor such as “Canonical” and “Non-canonical”, therefore it would be a great idea to include a youtube video to summarise these pathways and reinforce the in-depth description already provided on the page.
 
 

Negative aspects of the project and suggested improvements:
 
 

It was also noticed that a variety of terms were utilised which were not defined in the glossary such as “cyclins”, “pluripotent stem cells” and “ligands” for example. It is important to consider that the wiki should be able to teach at a peer level (criteria 4), as some students may not understand these terms. Therefore it is important to define them so audiences can develop a coherent understanding of the information. Another negative feature of the page was that it lacked interactivity. Indeed the page is very informative, however to further engage the audience, a suggestion would be to include a set of multiple choice questions at the end of the page which tests peers about the content covered.
 
 
It was also noticed that the page had a very limited number of subheadings regarding Notch’s involvement in embryonic development. A possible improvement would be to investigate Notch’s involvement in organ systems other than Cardiovascular and central nervous system. This will add a greater variety to the page and provide a greater depth of understanding regarding the role of the Notch signalling pathway in embryonic development.

 
 

===Group 2 Peer Review===
At first glance, I was blown away by your team's page. Definitely very impressive and understandable. The key points relating to the Notch signalling process are definitely clearly described however I may recall Dr Hill requesting that teams steer clear of clinical effects of genes(citation needed!). The choice of headings, sub-headings and diagrams show more than a good understanding of the topic area, it may be useful to include a table that summarises the various aspects of the Notch pathway so that readers realise there are different receptors. The content is cited correctly, however, I would not mind reading 'et al' instead of 'and colleagues' more often, I got sick of reading 'and colleagues'.

The information presented is mostly peer friendly in the context of a simple introduction but your glossary certainly needs updating, there are a lot of terms that a lot of students would not understand and a comprehensive checking of your page will offer you a list of words that you need to define. Also lacking are sketches presented in your own hands, instead of reusing published images. There is plenty of evidence that suggests your team has went beyond the formal teaching activities. In the context of the aims of the embryology course, you guys have emphasised the embryonic role of Notch but the aspect of developing technologies appears to have been ignored to an extent.

Overall, you guys have done a very impressive job that only requires minor tweaking, namely slight editing in the context of in text referencing, more comprehensive glossary as well as checking the course aims of embryology to incorporate the second criterion regarding technology. Excellent work!
===Group 2===

Well done on the progress you have made thus far! You guys have chosen appropriate headings and subheadings that effectively break down the Notch signalling pathway. A coherent introduction has been provided, giving a taste of what is to be expected in this project. The use of a table to explore the history of this signalling pathway was particularly useful in making the information understandable and relevant. Though you have done an excellent job, was there any reason you stopped at 1989? It may even be useful to create a brief timeline of events, thus allowing you to better explore current areas of research by considering past studies that have been performed.

You’ve provided a good overview of the canonical pathway with the appropriate use of a diagram which aids reader’s understanding of the information provided. In saying this, I think it would be useful to expand on how this pathway is tightly controlled, is it through transcriptional regulation or through other means? In addition, it may be useful to explain the differences in the non-canonical and canonical pathways in terms of their significance and role in embryonic development. I’ve noticed that you have provided a general overview of the role of Notch signalling pathway in embryonic development, do these roles differ between the canonical and non-canonical pathways?

In addition, it’s good that you have included the role of the Notch signalling pathway in animal development as it explores the scope of this pathway beyond human embryology but it may also be useful to explore animal models in research, especially considering that the ‘first description of a “notch” defect’ was discovered in Drosophila. By combining the role of animal models in expanding our knowledge of the Notch signalling pathway with the effect of this pathway in animals, it provides a more rounded approach to explaining and discussing this signalling pathway.

I particularly like how you have included statistics in the ‘Abnormalities of Notch signalling’ section as it provides insight into the importance of this pathway in embryological development. You have successfully described the type of mutation that results in the particularly disease in most cases except for Alagille syndrome. More detail in how the mutation causes the syndrome would be useful with an explanation of how the mutation is brought about.

Overall, you guys have done a fantastic job! You have appropriately referenced and cited all the information provided and have included useful flowcharts, tables and diagrams that aid understanding of the text provided. Providing more detail to each of the sections and communicating with all your team members in the discussion page will ensure that you produce an excellent project! Good luck!

===Group 2 Critical Assessment===

A job well done with the introduction! The introduction is brief however manages to link the topic to embryonic development, different medical conditions, whilst also outlining the function and elements of the pathway. Being brief and succinct, it allows the viewer to continue exploring the page without experiencing confusion at the first lot of information. Further to this, the history of the pathway is formatted well and is not too overwhelming or boring. It is evident you have decided ‘Current Areas of Research’ will also be included in your page which is a great idea as you have included a section on History. This would ensure your Wiki flows well, and covers the pathway from start to finish.

Images have been included to visually represent the elements of the general pathway, as well as the elements specific to the pathway in cardiac development, which forms a great aid for viewers in understanding the content. Videos explaining the different canonical and non- canonical pathways could also be included for viewers with a video learning preference.

Use of in text citations neatens the layout of information and enables viewers to access the article should they find the point interesting. Numerous subheadings have been included which further break down the page into small sections of information. This is a fantastic positive as viewers can locate information in which they are interested in easily instead of having to read through long paragraphs of text. I feel as if linking the topic clinically is extremely important which you have done a great job in! Along with the text explaining the disease, you could possibly include a table stating the disease, the mutation, and the symptoms for viewers after a more easy, accessible format.

Throughout the topics covered, a lot of jargon is utilized, however a full glossary has not been provided. A glossary should definitely be included for terms such as ‘gastrulation’, ‘kinases’ or ‘cardiogenesis’ in order to satisfy criteria 4. Additionally, the page does not cater for viewers interested in further reading up on the topic. To ensure criteria’s 4 and 5 are met, links to interesting facts or articles could be provided so the audience has access to more information if they would like to further their understanding. With a few improvements this Wiki page can definitely prove helpful in understanding the pathway!

===Group 2 Peer Assessment===

Your project is quite good and seems to be on the right track. All your references have been done in-text and have made it really easy to make one’s way to the research article to read more about certain points. Not only that, you have appropriately abbreviated your terms by using the full name initially, and I can see that you have a glossary section which should be beneficial in the future when more terms are added. Your history section is well presented but, it might be important to add references to the papers of the main points of discovery in your history section as to allow people to easily access and find the full article regarding the discovery.

The fact that you have added pictures is quite handy when it comes to using it as an aid to accompanying passage. With regards to the image legend, maybe add more information to it or transfer the description of the image present when clicking into the image onto the legend as to better represent what the image is about while having the passage right next to it. Furthermore, maybe it would be beneficial to add other forms of media such as videos to compliment the passages as well, and help better engage the reader in the topic.

With regards to your section on the canonical pathway, I’ve noticed that the specific genes that are targeted by Notch have been left out and I feel that it is important to mention those genes targets explicitly there as well. That being said, they are mentioned in the proceeding section so it isn’t imperative that you do this. Maybe also try seeing if there is any literature on how the NOTCH receptors come about, such as what genes transcribe it and how the protein is processed and expressed before signalling in the pathway can occur.

I think for the most part there is very little to improve with your wiki page given the quality of it albeit a few minor corrections that I have mentioned above. It is very concise and at no times do I feel that I am reading a wall of text that is disengaging. Thus I feel that as long as such quality is maintained then your wiki page will be quite good when finished.

===Group 2 – Notch Signaling Pathway ===
First impressions of Group 2’s page on the notch-signaling pathway are all positive. Subheadings are very well defined. They have chosen to include a brief yet informative introduction on the pathway, a simple table outlining the major scientific developments over the last 100 years, the molecular mechanisms of the pathway, its specific role in embryonic development (which they have further defined as cardiovascular and CNS), role in animal development, abnormalities relating to this pathway and a glossary. I think another positive aspect of this project, is that they have identified additional subheadings for which they are still to do research on; a particularly important one is current areas of research which not many groups have included. Furthermore, additional positive aspects of this project include the addition of images on the canonical notch signaling pathway and its role in cardiovascular development (which both appear also to be appropriately added to the website), which support the text nicely. It might also be useful to find a relevant video to include just to break up some of the text, and help make the page more interactive. It appears this group has widely researched their topic using both primary and review articles, which are all appropriately referenced using in-text citations. All of these aspects help to clearly convey the necessary information to the reader, and fulfill much of the required criteria of this project. In terms of their written information, Group 2 has included really detailed information on its role in embryonic cardiovascular development, as well as identifying some of the major research articles that have lead to these discoveries and a little bit about them (which then the reader if they are interested it can go read thanks to the inclusion of the in-text citations.) They do include a section of the roles of this pathway in animal development, which is really interesting and goes beyond the normal scope of this course.

Some negative aspects of the project include that, as part of the criteria being that the project has an “element of teaching at a peer level using the student's own innovative diagrams, tables or figures and/or using interesting examples or explanations” perhaps it would be useful to consider including a hand drawn image when researching the non-canonical pathway or transcriptional regulation of notch signaling, or even of some of the receptor/ligands involved in this signaling pathway. Furthermore, on a similar note it may be important to summarise the receptor subtypes involved in the different pathways, their role in embryonic development and abnormalities of the receptor subtype specifically relating to embryonic development in a table or dot point format. Additionally perhaps more information on its role in the CNS (or other systems during embryonic development) even if its not as detailed as cardiovascular, may help to inform the reader of all of its various roles.

In conclusion, it appears that this project is one of the strongest, it has very clear and informative subheadings separating well researched written material, supported by images sourced from the Internet. The main criticisms were just including your own innovative diagrams or explanations, videos to help make it more interactive and table or dot points summarizing the different receptor subtypes involved in each pathway. Following the completion of this, and the subheadings yet to be researched (and glossary) it appears that this project is going to be very successful in informing peers about the said pathway.

===Group 2 Peer Assessment===

Positive Assessment:

So far this page looks great and very organised. I am really impressed by the set out of the information and the way the headings are arranged. It made it really easy for me to navigate around for particular information and not have to look for around aimlessly when I was looking for something in particular. Furthermore I think that the actual categories/sub headings used so far are very concise and effective. For example, I appreciate the brief introduction along with an overview of the molecular mechanisms involved in notch signalling before introducing its roles in embryonic development. This way I was able to have a understanding of what is really involved before understanding how it is important in embryonic development.

The references are also very neatly and correctly done and many times when I did not fully understand a concept I clicked on the citations which took me to the relevant articles and my understanding was clarified. I also really enjoyed the commentary on the specific research papers, for example cardiomyocyte specification and differentiation where you guys actually compared information from separate studies to make the information more whole and relevant.

In the abnormalities section, I think it was really awesome you guys included so many statistics and symptoms and not just a description of the abnormality.

Critical Assessment:

Although everything looks really amazing a couple of improvements that I personally think could be made would make this page really useful to students.

The introduction, although very informative can be simplified a bit more to address criteria 4 and make it a bit easier to understand. This can be done through including an interesting or very simplified diagram to engage the student from the beginning. I would also generally include more diagrams and drawings that are personally drawn as the pictures used although effective, can be difficult to understand when you are learning for the first time. It would also be nice if more words are included in the glossary because there was a quite few words I did not know the meaning of.
Lastly I think it would be a great addition to your page to include another subheading which outlines how the abnormalities are treated as this is something that I was intrigued to discover.

Overall I think your page is going great guys keep it going !

===Project 2: Notch signalling pathway===
====1. The key points relating to the topic are clearly described.====
There are headings for key points and the information for these key points has clearly described. This information is laid out in a clear way beginning with an introduction, historical aspect of the topic and continues to more specific information (e.g. animal models) related to the overall topic.

====2.The choice of content, headings and sub-headings, diagrams, tables, graphs show a good understanding of the topic area.====
The Notch singalling pathway has a very clear contents list. This demonstrates that a lot of thought and research has gone into the topic. There are two figures which are very neat and well set out. These are referenced. There is one table which described the historical aspect of this topic and this is very clear and beneficial as it summerises a lot of information in a clear manner.

====3. Content correctly cited.====
The content is cited correctly. If the refernces are used more than twice this has been cited in following the Wiki guidelines and the reference is not repeated in the list.

====4. The wiki has an element of teaching at a peer level using the student's own innovative diagrams, tables or figures and/or using interesting examples or explanations.====
This wiki does have an element of teaching: It is clearly laid out, it is easy to read and the information is set up in a correct manner with a general overview, historical aspects and then more precise information is given. There is some interesting examples given which describes abnormalities in this pathway.

====5. Evidence of significant research relating to basic and applied sciences that goes beyond the formal teaching activities. ====
This is very much evident. There is evidence that research has been undertaken as the topic has been divided into sub topics and there is a lot of interesting clear information to educate the reader.

====6.Relates the topic and content of the Wiki entry to learning aims of embryology. ====
Yes the topic does related to the learning aims of embryology and how Notch signalling pathway is involved in embryonic organ development through the regulation of cell-cell signalling

====7. Clearly reflects on editing/feedback from group peers and articulates how the Wiki could be improved (or not) based on peer comments/feedback. Demonstrates an ability to review own work when criticised in an open edited wiki format. Reflects on what was learned from the process of editing a peer's wiki.====
This is still not as evident as there is no comments or feedback observed. There are still some sections that have information missing and perhaps comment or feedback could have been given here to ensure that the students fill in this missing information or remove the subheadings all together.

====8. Evaluates own performance and that of group peers to give a rounded summary of this wiki process in terms of group effort and achievement.====
The way this Wiki is laid out clearly demonstrates that there has been some feedback and communication between the group. It seems that each member of the group did write a section, yet the sections do come together and do not seem out of place. However there are sections with information missing and this needs to be addressed.

====9. The content of the wiki should demonstrate to the reader that your group has researched adequately on this topic and covered the key areas necessary to inform your peers in their learning. ====
Yes the Wiki content does demonstrate that the group has researched adqueately in this area.

====10. Develops and edits the wiki entries in accordance with the above guidelines. ====
This has been achieved. This wiki entry does seem to be in accordance with the guidelines provided.

[[User:Z3462474|Z3462474]] ([[User talk:Z3462474|talk]]) 07:15, 23 September 2016 (AEST) Hey no worries I hope you feel better soon! I won't be able to do as much during the midsem break which is why I've been doing lots this week. I'll have a look at that link thanks! Also I tried to make a Glossary but am having trouble with the coding side of it but I'll try fix it later to make it a proper glossary :)

 
[[User:Z5015014|Z5015014]] ([[User talk:Z5015014|talk]]) 21:00, 22 September 2016 (AEST) I'm so sorry I've been terrible with putting stuff on our page!! I know I said I would get some done this week but I've been sick these past few days and still recovering so I probably won't make it to the lab tomorrow. I'm having some trouble finding an image that summarises Notch signalling that we can use (most of the good ones I've found don't allow reuse) but I'll keep looking. I'll definitely do a lot more during the midsem break. sorry again! I also found this link: http://www.omim.org/entry/190198 that looks like it has some really good references for different roles in development.

[[User:Z5015014|Z5015014]] ([[User talk:Z5015014|talk]]) 14:27, 16 September 2016 (AEST) looks like a great picture so I think we can leave it. I just altered the formatting of the image a little bit, but feel free to change it back if you prefer the previous placement! also I think having the copyright info on the file page is enough. thanks for doing that, I'm still hunting out pictures as well. I've been busy this week with another group project but now that it's out of the way I should be able to do a lot more here. :)

[[User:Z3462474|Z3462474]] ([[User talk:Z3462474|talk]]) 09:21, 16 September 2016 (AEST) I found one that didnt look too complicated and also found that it allowed unrestricted use so I've added it into the cardio section of our page (we can always delete it later if need be), not 100% about my formatting though and whether I should include the legend/copyright notice directly on our page? If you click the image though its all there :)

[[User:Z5015014|Z5015014]] ([[User talk:Z5015014|talk]]) 23:08, 12 September 2016 (AEST) I've been looking around and found some images, but most of the time they involve a lot more detail than we need and I don't want to overcomplicate it. will keep researching this week and see if I can find some simpler diagrams. :) The images in that book look really good but yeah I'm not sure what the copyright details for that are. if it comes to it I think if we reproduce it by hand and credit the source then it's fine!

[[User:Z3462474|Z3462474]] ([[User talk:Z3462474|talk]]) 13:50, 12 September 2016 (AEST) Has anyone found any good images to use for our page? I have found a couple of diagrams on cardiac development and Notch in this book chapter: http://www.sciencedirect.com.wwwproxy0.library.unsw.edu.au/science/article/pii/S0070215310920115 but am still looking to the copyright restrictions etc and thought I'd check everyone's opinion

[[User:Z3462474|Z3462474]] ([[User talk:Z3462474|talk]]) 09:22, 9 September 2016 (AEST) Hey everyone, I have added some of my notes to the main page, they are still a work in progress though! I'll continue to research the roles of Notch in the development of the different systems

[[User:Z3462474|Z3462474]] ([[User talk:Z3462474|talk]]) 10:04, 2 September 2016 (AEST) Just found this online textbook titled 'Notch Signaling : Methods and Protocols' http://www.springerprotocols.com.wwwproxy0.library.unsw.edu.au/BookToc/doi/10.1007/978-1-4939-1139-4

This one also looks like it might be helpful: http://www.sciencedirect.com.wwwproxy0.library.unsw.edu.au/science/bookseries/00702153/92

[[User:Z3462474|Z3462474]] ([[User talk:Z3462474|talk]]) 14:27, 26 August 2016 (AEST) Here are some reviews I have found that could be a helpful starting point:

Notch signalling at a glance: http://jcs.biologists.org/content/joces/126/10/2135.full.pdf

Signalling pathways for neural development: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369499/pdf/WJSC-7-437.pdf

Notch's role in diabetic neuropathy https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3677813/pdf/nihms473246.pdf

Notch in cardio development and disease http://circres.ahajournals.org/content/118/1/e1.full

[[User:Z5015014|Z5015014]] ([[User talk:Z5015014|talk]]) 14:28, 26 August 2016 (AEST) here's the embryology site page for [[Developmental Signals - Notch|Notch signalling]]!

[[User:Z5015014|Z5015014]] ([[User talk:Z5015014|talk]]) 14:31, 26 August 2016 (AEST) I also found a review article for Notch signalling in the common fruit fly, which could be a good idea for a subsection: PMID 12369105 ''General outlines of the molecular genetics of the Notch signalling pathway in Drosophila melanogaster: a review''.

[[User:Z5015014|Z5015014]] ([[User talk:Z5015014|talk]]) 14:44, 26 August 2016 (AEST) and here's some more reviews: PMID 22397947 ''Non-canonical Notch signaling: emerging role and mechanism'' and PMID 21828089 ''Notch signaling: simplicity in design, versatility in function''.

[[User:Z5014803|Z5014803]] ([[User talk:Z5014803|talk]])
https://www.researchgate.net/publication/264164124_Introduction_to_Notch_Signaling This seems like a good link for the history and discovery of the pathway

[[User:Z5014803|Z5014803]] ([[User talk:Z5014803|talk]])
https://embryo.asu.edu/pages/notch-signaling-pathway-embryogenesis Can be used for introduction

[[User:Z3462474|Z3462474]] ([[User talk:Z3462474|talk]]) 12:41, 19 August 2016 (AEST) Signalling in neural embryonic development looks interesting! Particularly the paper about NSCs and psychiatric disorders.

[[User:Z5015014|Z5015014]] ([[User talk:Z5015014|talk]]) 21:59, 18 August 2016 (AEST): Hedgehog signalling (specifically SHH signalling) sounds really interesting!

[[User:Z5014803|Z5014803]] ([[User talk:Z5014803|talk]]) 22:39, 18 August 2016 (AEST): Bone Morphogenetic Proteins (BMP) signalling in development looks interesting

[[User:Z3491219|Z3491219]] ([[User talk:Z3491219|talk]]) I think looking at how in utero exposure to cigarette smoke affects fetal ovarian development signalling would be interesting.

===Group 2===
This web page is developing very well, with comprehensive information and textual information. Relevant images and diagrams have been included and accurately referenced, which is to be commended. Student produced images, diagrams and flowcharts should also be included to reflect depth of knowledge on this topic. More images would enhance the readers’ understanding of topics like the development of the Atrioventricular Canal, heart valve and outflow tract, all of which are subheadings. Short movies and animations should also be included to assist the readers in visualising these signalling pathways and embryological developments being discussed. An interesting and potentially humorous image could also be included at the beginning of the web page to attract the reader’s attention and add interest to the page, such as an image of an ordinary notch at the top of the page.

The subheadings included in this web page are appropriate and have been well organised, ensuring consistency and cohesiveness in this project. The introduction is well written, as it covers a range of topics including an overview of the role of the Notch signalling pathway as well as an introduction to the abnormalities associated with mutations in the functional components of the pathway. The timeline could also be improved by including developments in research over the last 20 years, as well as the direction current research is moving in and where future research could be headed. An elaboration on 1914 by further explaining why this is called the “Notch signalling pathway” with the aid of an image would also be useful. More information on John S. Dexter and his research process, his team and initial findings would also add depth and interest to the web page. Another table could be included in this web page to help the readers differentiate between the four Notch genes in Mammals, including further information on each gene, their respective locations on chromosomes, functions and an image of each if possible. The location of the locus of the Notch gene on the 3C7 band of the X chromosome is included, as well as the NOTCH3 located on chromosome 19p13, showing detailed knowledge and extensive research by the group. Images, potentially student drawn, of where these locations physically are would also reflect a deeper understanding.

The ‘Roles in Embryonic Development’ section and its respective subheadings have also been well organised and structured. There are several headings in this web page that require completion before the submission date, including the ‘non-canonical pathway’ and ‘transcriptional regulation of notch signalling’ headings. More animal models can also be included, with the subheadings in this section also requiring completion. An abnormalities section has also begun well and is detailed and well referenced. It still requires completion as some of the sub-headings are still empty. Images of symptoms of these abnormalities such as the rib and spine abnormalities associated with Spondylocostal Dysostosis, and the eye conditions and facial features associated with Alagille syndrome would add depth to this section. A glossary section has also been started, but can definitely be added to to improve the understanding of the readers. Terms to be added could include proteolytic reactions, ligands and descriptions of signalling molecules such as MyoD, Mash1 and GATA2.

Referencing has been carried out well, with in-text referencing throughout the web page. The introduction was well referenced, as well as the “Roles in Embryonic development”, “Animal Models” and “Abnormalities” sections. However, no in-text referencing has been carried out for the “Overview of Molecular Mechanisms” section and the timeline. This should be resolved as soon as possible so that external links are easily accessed by the readers should they want to seek further information. Complete and proper referencing would also satisfy one of the criteria of this assessment, that the content is correctly cited and referenced.

User:Z5015337

2016-10-06T23:58:13Z

Z5015337: /* Lab 9 Assessment */

Talk:2016 Group Project 1

2016-10-06T23:29:11Z

Z5015337:

{{ANAT2341Project2016discussionheader}}
=Peer Review=

===Peer Review - Group 1===
You guys have done really well to accumulate a lot of relevant information so far on your wiki page which is definitely a positive for your team. In the context of criterion 1 of the assessment criteria, I am not certain that the key points are clearly described as of yet, there is just a lot of information that is not presented to the reader in a targeted manner, so this definitely needs some work. As I have stated previously the choice of content appears to be adequate to address your topic however you guys need to work on increasing the number of subheadings as well as providing an introduction as the project aims remain unclear. Content is not completely correctly referenced yet, presumably due to the fact that you guys are still making your project page up but referencing is very easy to do correctly on this wiki and I implore you to make sure it is done correctly when it is time to submit the assignment.

As I have alluded to previously, elements of teaching at a peer level were completely missing in this and these definitely need to be addressed, probably by putting entries into your glossary as well as creating a well structured introduction. It would also help if you guys drew some representations of information, such as sketches of pathways. There is certainly evidence of going above and beyond the formal learning activities, which is a major positive for your project. In the context of learning objectives of the course, you guys are addressing the aspect of embryological development but have not addressed the relevance of new technologies in the WnT Pathway.

Overall, there is a lot of potential for you guys to put out a very good wiki page if you clean up your page so that it is more coherent and insert some information that is lacking so that a relatively uneducated reader could understand the WnT signalling pathway from the wiki page. Well done!

===Group 1 Peer Review===

'''Positive Factors'''

Group 1 have a clear allocation of sub topics between members of their group which is shown under the subheadings. The pathways (e.g. canonical pathway) are all described clearly, I was able to follow easily despite not having extensive knowledge on the subject. I think this could be even more improved with some diagrams or flow charts to support the written explanations. Another positive aspect of this Group’s page is how they have included information from studies under a separate heading to emphasise their findings in regards to Wnt. Moreover, there is a subsection that directly and clearly relates Wnt to the developing fetus.

'''Points for Improvement'''

Some improvements I would suggest would be: the formatting on Group 1’s page be tidied a little but since this is a draft it is still in early stages (more specifically, Group 1 could use uniform subheading sizes and uniform subsections/subtopics for each pathway described); also it would be great if the references were sorted under one heading at the bottom of the page; and a short generalised introduction could be added to inform readers of the general role of the pathway and some information about relevant molecules.

'''Overall'''

Overall the main strength of Group 1’s page is the clear explanations they have provided, which I think is really important for meeting the assessment criteria for this project. More specifically, criteria 1, 5 and 6 have been addressed so far by this Group. With a few improvements to formatting and layout this page will provide a great resource for understanding the Wnt signalling pathway.

Group 1:
 
 
Positive aspects of the project and suggested improvements:
 
Upon assessment of this project, it appears that the authors have devised a variety of subheadings related to the signalling pathway of the Wnt receptor in embryonic development which is excellent. The group has also began investigating the involvement of Wnt in numerous aspects of embryonic development such as skin formation. The use of subheadings and headings related to the Wnt receptor partially meets criteria 1 and 2 assessment. It also appears that the group has cited and referenced sources for some of the information utilised, particularly when describing the “Caronical Pathway”. This also partially meets criteria 3 for this assessment. The group has also attempted to explore abnormalities in the Wnt pathway by describing interruptions in the pathway and its relation to cancer which is very interesting. They have therefore attempted to research ideas related to this receptor that extend beyond formal teaching activities, by explaining the link between Wnt abnormalities and disease (criteria 5).
 
 
Whilst there are the positive aspects of the page, improvements can still be made to ensure that the group satisfies the first five points of the marking criteria. Firstly, although there appears to be subheadings, there only appear to be few and therefore it would be excellent to add more subheadings. Subheadings may relate to the history of the Wnt signalling pathway or even subtypes of the receptor as well as their respective functions. In addition, whilst the group appear to have cited some of their sources, it is important to cite all sources, particularly when gathering data under the “Non-canonical pathway” subheading. Although a series of articles have been referred to, it is vital that the group includes in-text citations in order for the audience to determine the source for each segment of information. A suggestion would be to investigate more examples of diseases caused by abnormalities in the Wnt signalling pathway
 
 
Negative aspects of the project and suggested improvements:
 
 
The group appeared to provide a general description of the abnormalities associated with disruption of the Wnt pathway; however they did not talk about abnormalities in the context of embryonic development. A suggestion would be to discuss Wnt abnormalities to the effect it has on embryonic development. It was also noticed that the group failed to include diagrams, tables or figures to reinforce the information. The use of diagrams would assist the audience in developing a visual understanding of the information presented and also makes the wiki page more appealing too. Therefore, a suggestion would be to use diagrams and figures. For example, a diagram of the signalling pathway would be a suggestion. It was noticed that the page appears to have no introduction or history describing the Wnt receptor. Therefore, a possible improvement would be to include a brief introduction and history at the beginning of the page as well as a few diagrams to provide the audience with an insight into what the receptor’s purpose is before exploring its function in embryonic developing.
 
 
In addition, it appears that the group has focused on the role of Wnt in skin development of the embryo only. A possible improvement would be to investigate the involvement of Wnt in other areas of embryonic development, perhaps the development of specific organ systems or other structures.
 
 
 
 
 
 
To all group members:
*More info on pathway focusing on fetus development, and which pathway it is majorly part of - focus research on those body parts
*Make your section presentable
*At least one picture per section

===Group 1===

You guys have made significant progress on your project, managing to touch briefly on each section of your assignment. There have been some good choices of subheadings but I think some improvement can be made. For example, I think it would be useful to breakdown the general heading of ‘introduction’ into smaller subheadings so readers are made aware of what will be discussed in this section. It would also be useful to touch upon the importance of this pathway and thus, highlighting its significance in embryological development.

In terms of the content of the project, being only in the draft stage a considerable amount of editing is required. For example, there has been mention of the TCF/LEF family and though the use of this abbreviations is useful, I think it would be appropriate to initially include the full name and explain this term in brief detail. In addition, there has been discussion of the ‘canonical’ and ‘non-canonical’ pathways of WnT Signalling Pathway but you could consider discussing the significance of having these two separate pathways. Comparing and contrasting these two pathways may also assist in aiding one’s understanding of the topic.

Though it is great that you have made progress, I think more detail is required in each section, particularly in linking the effect of these pathways on embryological development. Also, greater attention needs to paid to referencing and utilisation of studies that have dissected this signalling pathway. For example, greater emphasis can be placed on studies performed on ‘embryos of Xenopus laevis’ or the in vitro experiments on mice. Instead of saying ‘a study’ or ‘another study’ acknowledge the researchers of this study as it will increase the validity of your argument while providing readers with the opportunity to refer back to these papers for more information if required or interested. More detail is also required on the effect of this pathway on skin formation. One way this could be done is by expanding on the information already provided, for example, explain how ‘WnT signalling inhibits the ectoderm’s responsiveness to FGFs’ and provide a detailed explanation of the feedback mechanism. Though your topic is focusing on ‘WnT Signalling pathway in the skin of fetus’ It would be beneficial to explore the roles of Wnt signalling in other areas of embryological development as this could provide insight into the abnormalities caused by mutations in this pathway. In terms of the ‘what can go wrong’ section, try breaking this segment into the various embryological deficiencies that can develop through disruption of the WnT pathway and try and make it relevant by providing statistics.

Overall, you guys have done a fantastic job! It was good to see that all group members had contributed to the project. The main thing that requires improvement is the lack of detail. Through editing and inclusion of appropriate references and citations you can significantly improve the quality of your work. It would be useful to add some diagrams or images to help explain the pathway. In addition, try utilising your discussion page and communicating with your other team members. By providing feedback and suggestions you can assist in efficiently producing an excellent project. I hope this helps!! 

===Group 1 Critical Assessment===
In terms of the topic of WnT signalling pathway, the page is beginning to come together with a great amount of information. What I particularly like is how the different concepts introduced in the page have been explained, for e.g. the different WnT pathways. However the content for each pathway does not seem to be consistent. While the canonical pathway addresses the mechanism, the non-canonical one doesn’t. I would suggest constructing a table to compare the similarities and differences between the various pathways, and adding images or shorts clips with audio to represent the elements of the pathways in a different form. This would not only enhance the look of your page but also make it more interactive for the audience.

A great positive is to see links to research articles have been provided for the audience to access if they are interested to read on further. The links are short and easy to see, and direct you straight to the article on Pubmed, a reliable source. An effort has also been made to summarise the article, however the summary should be available as a simple breakdown so the audience can refer to it if they struggle to understand. The summaries include some jargon that can be further simplified.

In relation to criteria 1, the key points have definitely been highlighted and the signalling pathway has been associated with the fetal development, however to make it more interesting and satisfy criteria 5, possibly construct a table or briefly outline how WnT signalling is involved in other areas such as Type 2 Diabetes and Cancer. Furthermore, to relate the topic back to embryological development explore the pathway in other areas such as gastrulation, rather than limiting discussion to skin development.

Lastly to satisfy criteria 3, attempt to include in text citations within the paragraphs, instead of displaying references towards the end of the page. Overall, great job in gathering and highlighting key features, and backing up your information with relevant articles!

===Group 1 Peer Assessment===

The start you have made on your project appears to be quite decent. There seems to be a clear overview and scaffold of how your page will look and what it will discuss in the end. For the most part the usage of dot points has made understanding your points with regards to the signaling pathways (Canonical pathway section) a lot easier as opposed to having a wall of text. I would recommend possibly adopting dot points when explaining the pathway regarding the Wnt-Calcium Ion pathway to make it easier to digest. That being said though, there are areas within your wiki page that would most likely benefit from having complete paragraphs such as your sub sections labeled under the non-canonical pathway. It appears that each individual point in the sub section role appears to represent individual points that could be substantially elaborated on. In way I feel that it would make the ideas in the section less disjoint and more clear, given that writing in a paragraph format would be suitable for longer passages. Also for the part where there are there are research articles linked, and descriptions of such articles, it might be better to try integrate such ideas into other main components of your wiki page, because they seem quite out of context and out of nowhere. That being said you could also just put this under a current research heading and talk about it with respect to the current findings of the Wnt pathway.

Another main aspect that should be corrected is that in some sections, there is the assumption in your wiki page that the reader fully understands all your abbreviations. I know it sounds silly but it is probably best that your group coordinates or finds where you first use an abbreviation such as CaMKII in your non canonical pathway section and change it to the unabbreviated name, with the abbreviated name in brackets, where from there you can just use the abbreviated name. Also maybe just providing a glossary of the abbreviated terms and their unabbreviated terms at the end of your page will do as well. Also its good to keep in mind that you may have already done this for some terms, so look out for that as well.

With regards to your referencing, I see that it is quite extensive, but there seems to be a lack of in text citations. As a result, its quite hard for those who read your page to quickly find the appropriate citation with regards to the sentences or dot point being read. For the sections such as “Canonical Pathway: How it works” this isn’t too bad, as there is only one reference, but for the “Non-Canonical Pathway section” there are way too many for it to be easy to tell where the citations are associated to. So overall for this I recommend your group to use in-text citations. Also I’ve noticed that you have used a review to cite your whole “Canonical pathway: How it works” section, which for the most part most likely contains all your information you have stated, but doesn’t give credit to the specific or individual authors included in the review and also requires the reader to go and find the specific sections in the review that you have used to cite your text. It is such that it would be better to use research articles to site your individual points, maybe extracting such research articles from the review article itself.

Overall the start made on your project is appearing to take shape, where I see that there are many subheadings yet to be filled below the “Wnt-Calcium Ion pathway” section. I’m sure if your groups keep up the quality of the work, your page should turn out fine with the addition of incorporating the feedback I have provided.

===Group 1 – Wnt Signalling Pathway===
Positive aspects of the project include that fact that this group has included detailed information of the different WnT signaling pathways. It does seem however, that this information would perhaps be better conveyed to the audience if it were accompanied with images (either sourced from the internet or hand drawn) and/or videos/animations, as well as some information on the role of each signaling molecule/receptor subtype (perhaps in a table) just to provide a more thorough explanation of this pathway. Furthermore, this group has made a conscious decision to include a glossary, although they have not yet started this, it is going to be something the group can add to whilst finishing the project and will help the reader better understand the concepts they discuss. This group has included a large amount of references throughout their project, including a significant amount of recent primary articles, which shows the reader that their information is well researched and very current. However, the only criticism here is that they aren't appropriately formatted for the purpose of this assignment. I would suggest that in text citations would be more appropriate, so the reader can clearly identify where this specific information is from and then go directly to said source if need be.

Alternatively negative aspects of the project, which may need some revising before submitting the final version of this assignment, would be the formatting of the project as it appears relatively incomplete. Although there are some subheadings, which are helpful, it may be useful to add additional ones to these to make it a little clear for the reader. For example perhaps use a similar scaffold to the other group projects, which have included ones such as introduction, history, outline of the signaling pathway, its specific roles in embryonic development and then abnormalities specifically relating to embryonic development, as this would help break up the information better and make the projects more consistent for readers. Most of the work on this project seems to focus on explaining the signaling pathway so I assume its more the case of the group hasn’t got around to it yet, but I think more information on the role this signaling pathway specifically has in embryonic development is required, like the paragraph on early stages of skin formation, in order to tie in the assignment with what we have been learning in the labs and lectures. As mentioned I think the subheadings may need some revision, and the current ‘What can go wrong’ may be better described as ‘abnormalities’ that way you could also include a discussion of abnormalities to Wnt that specifically influence normal embryonic development, as well as still include the paragraphs on its influence on tumor cells which could perhaps be found using the ‘omim’ site searching by a receptor subtype or pathway. Also, although you have included more of a discussion of abnormalities that occur later in development, it is interesting for the reader and does go beyond our understanding from class, but the main focus probably should be on abnormalities in embryonic development.

In conclusion this project is definitely on its way to being really good, the information on the signaling pathways appears to be well research. The major criticisms were mostly focused on presentational aspects of the project like subheadings, references and the inclusion of images/tables. With some more research on its role in early embryonic development and abnormalities this will be very successful.

===Group 1 Peer Assessment===

Positive aspects of the project and improvements:

Upon initially glancing over the project you can clearly see a range on headings and subheadings and it is evident by these that the project is about the WnT signalling pathway in skin of fetus. This is sufficient for assessment criteria 1 and 2 as you can see the aspect of research they are targeting such as skin formation during embryonic development. Throughout the text you can see citations relating to the topic and a range of references at the end of the project. This satisfies the requirements for criteria 3 but just a small critique would be to put these references in the references section just to clear out the unnecessary area. It can also be commended that the group project goes above and beyond the curriculum of informing us about the background information of WnT signalling pathway in skin of fetus but also includes the complications and diseases arising due to abnormalities in the WnT pathway. This is excellent and satisfies the requirements for criteria 5

There can be some improvements in the project but they are not necessarily of the utmost importance. Firstly, the group can add other specific subheadings and the relevant information under them such as the history or background of the signalling pathway. This is just so the reader has a more rounded knowledge of the pathway and can increase the interest and keep them engaged. It would also be good to see in the text and not just at the end of a paragraph. Such as, in the canonical and non canonical pathway heading it would be recommended to have in text citation and not just at the end just to show the reader where the information was gathered from.

Negative aspects of the project and improvements:

Although the project has a fair amount of positives there are some areas that are lacking. Firstly, the report requires additional information in each section and how this information can be linked to pathways in embryological development. It would also be recommended to put in diagrams, images, tables etc. This would engage the reader and make the read more interesting since at the moment there are no images or tables. Also doing so will satisfy one aspect of criteria 2. This way the audience can develop a visual understanding of the topic. It would be advisable to put tables in the history section in the form of relevant dates/years and the information corresponding to the year.

Also, it would be good to see the role of WnT signalling pathway in something other than skin, for eg: an organ or tissue or cell. This would aid in achieving a higher mark for criteria 5 as you go above the required information. Overall it was great to see all group members contributing to the project but minor edits such as citations, images, tables, and adding additional information to sections would really captivate the reader and make it an enjoyable read.

===Peer Assessment: Project 1: WnT Signaling Pathway in skin of fetus===

====1. The key points relating to the topic are clearly described====
There are headings for key points but the information for these key points has not been added so far.

====2.The choice of content, headings and sub-headings, diagrams, tables, graphs show a good understanding of the topic area.====
The WnT Signaling pathway wiki does have a list of contents, which demonstrate that the topic is divided into different section. However it is clear some thought has gone into this. However this is not finished, there are not tables, diagrams, graphs and a lot of work is needed.
There are sub headings but there is no clear concise information under these headings. There is no introduction on what the topic is about and this makes the reader a little confused. There are a lot of parts missing and not filled out.

====3. Content correctly cited.====
The content is not cited correctly. There is a reference section but there are no publications that have been cited listed.

====4. The wiki has an element of teaching at a peer level using the student's own innovative diagrams, tables or figures and/or using interesting examples or explanations====
There are no graphs, diagrams or tables and these clearly will help the reader have a better understanding of what the wiki is about. There does not seem to be any examples or explanations that show the students own innovation.

====5. Evidence of significant research relating to basic and applied sciences that goes beyond the formal teaching activities.====
This is somewhat evident but there is not enough clear information and it makes it difficult for the reader to follow the topic.

====6.Relates the topic and content of the Wiki entry to learning aims of embryology.====
There is a section on foetus skin formation and this will be interesting to read however it is still not finished. Figures and diagrams would aid a lot to visualize this section.

====7. Clearly reflects on editing/feedback from group peers and articulates how the Wiki could be improved (or not) based on peer comments/feedback. Demonstrates an ability to review own work when criticised in an open edited wiki format. Reflects on what was learned from the process of editing a peer's wiki.====
Each section has been divided amongst the group but it seems that the members of the group have not really communicated or finished their own sections. This is not clear at all. The Wiki has a lot of room for improvement, the group needs to meet and decide who will do which section, the participants of the group need to find review publications and summarise this information for each section. Also it is a good idea to see how these projects were edited in the previous years and this will help with the layout.

====8. Evaluates own performance and that of group peers to give a rounded summary of this wiki process in terms of group effort and achievement.====
The content of the wiki should demonstrate to the reader that your group has researched adequately on this topic and covered the key areas necessary to inform your peers in their learning.
This is not demonstrated and it seems that the key areas have not yet been researched adequately. There is still a lot of information missing and the overall flow of this wiki is muddled.

====9. The content of the wiki should demonstrate to the reader that your group has researched adequately on this topic and covered the key areas necessary to inform your peers in their learning.====
The key areas on this wiki have been set up but there is no clear and adequate information that is correctly cited at all. It is a very poor effort thus far in terms of group research.

====10. Develops and edits the wiki entries in accordance with the above guidelines. ====
This still has not been achieved at all. There is no editing and it seems the group has put little effort in this project.

==Notes==
Just trying to simplify and understand the process and these are some of my notes !(z3417363)

The inactive Wnt Pathway In a normal cell:

In most normal cells the Wnt pathway is inactive. In the cytosol , the destruction complex is formed from the proteins beta catenin, GSK3 beta, Axin,APC, Ck1-alpha. The ubiquitin ligase beta TRCP is able to bind to beta catenin and transfer short ubiquitin peptides to beta-catenin. In other words the beta-catenin is phosphorolated and this beta catenin can then bound and be by a complex of protease (proteasome) . Thus a low level of cellular beta catenin is achieved.
Therefore no beta catenin reaches the nucleus and the transcription factor of the TCF LEF family along with other proteins (groucho) binds to DNA and inhibits gene expression.
So essentially when WnT is inactive, beta canenin is destroyed and does not reach nucleus and transcription is inhibited.

The Active Wnt Pathway in a normal cell.

Extracellular(outside cell) Wnt binds with the membrane receptor frizzled (FZD). The wnt pathway is activated and activates the cytosolic protein "dishevelled"(DSH) which induces dissociation of the protein destruction complex. Because the protein complex is destroyed beta- catenin is no longer modified by unbiquitin peptides/phosporolated and is not destroyed. Since the supply of beta catenin continues the level of beta catenin rises, first in the cytosol and later in the nucleus. Once the beta catenin reaches the nuclue it binds to the TCF LEF transcription factor which changes them from a transcriptional repressor into an activator. TCF itself activates an RNA polymerase which induces gene transcription.
So essentially WnT starts gene transcription by allowing beta catenin to reach the nucleus.

This is actually very similar to a tumour cell where the mutation of the protein complex also inhibits the destruction of beta catenin and allows it to grow in quantity and reach the nucleus and start gene expression. However this is not uncontrolled and can be compared to a car travelling with no brakes. Ultimately this abnormal proliferation leads to malignant adenocarcinoma (cancer).

Use pubmed, biomedcentral journals==you can find it on pubmed just plug in the title and you will get the pubmed number>BMC developmental biology journal, journal of cell biology(cant use last 6months of research), proceeding national academy of science(can only use after 6months), public library of science omim
include research labs, animations
use the help tab
where the terminlogy came from
this is a student drawn image , based upon and give the reference

=== Group 1===
GROUP 1
A great start to this group project has been made, with a substantial amount of textual information. No images have been included, limiting the visual engagement of the readers. The signalling pathways discussed extensively in the text would be easier to understand if images as well as diagrams and flowcharts were included. These flowcharts could summarise the processes in the Canonical and non-canonical pathways, as well as the Planar cell polarity pathway, the PCP pathway and the Wnt Calcium pathway. Since a range of pathways are described in this web page, it is essential that diagrams are included to simplify these, allowing the audience to consolidate their knowledge of these processes. Another addition could be short movies that would aid in the visualisation of these processes. Student drawn images should also be included to reflect the depth of knowledge of the individuals producing this web page. An interesting and potentially humorous image could also be included at the beginning of the web page to attract the reader’s attention and add interest to the page. One of the criteria to be fulfilled is that the wiki has an element of teaching at a peer level using the student's own innovative diagrams, tables or figures and/or using interesting examples or explanations. Hence, making these additions to the page would satisfy this criteria.

An extensive list of references have been included throughout the paper. However, no in text referencing has been carried out. For example, at the end of Caroline’s sections, references including PMIDs have been included, but the lack of in text referencing means that the specific papers used for each piece of information can not be easily identified by the reader for further reading. Other members of the group have also placed their references at the end of their respective sections, rather than using in-text referencing. Compiling all the references at the end, after in-text referencing has been completed, will improve the cohesiveness of the paper, rather than having a separate list of references for each section. This would also improve the organisation and aestheticism of the page. One member of the group has commented “I’m not sure how to reference things that aren’t from pubmed” on the page. The solution to this problem would be to either ask fellow group members and colleagues from the class, or to ask Dr Hill as to how he would like these references to be made, ie. which style of referencing he would prefer. Other good resources such as OMIM have been identified, which is commended, and looking in places other than PubMed will create an extensive reference list and a range of information from various sources. This would fulfill the criteria that the page should demonstrate that the group has researched adequately on the topic.

Subheadings have been included, organising the web page well. Names of the group members should be removed from subheadings when possible as these are visually distracting and unnecessary. Some subheadings also have not been formatted correctly, such as the “===What can go wrong?===” subheading, which needs to be fixed so that it is formatted in a similar manner to the other headings. More coherent formatting could also created in combining Tony’s “Abnormalities” and Arsalan’s “What can go wrong” sections. Many subheadings need completion with more information, including the “WnT-Calcium Ion Pathway - Tony”. In this section, the dot points “abnormalities”, “main components” and “functions” dot points should be made into subheadings and completed. The “Studies” section should also be elaborated on with more textual information, including specific researchers and dates. This section could be developed into a timeline of the history of the research associated with WnT signalling pathways, presenting this information in an accessible and interesting manner. A wide range of research has taken place, evident in the extensive list of references at the bottom of this section. This section can be enhanced by referencing other studies more specifically by naming the scientists involved, and when this research was carried out. This would be better than referring to research as “a study”. Ensure in-text referencing is carried out effectively in this section so the readers are able to easily find these research papers should they require more information.

The “Things to do/reference” list at the top of the web page should be resolved as soon as possible so that these notes can be removed from the top of the web page so that the page can begin with relevant information. The comments and dates at the top of the web page shows a progression of this project over time as well as group communication, which is commended. The glossary section should also be developed at the bottom of the page to contain definitions for words like glycolipoproteins, the TCF/LEF family, abbreviations like CaMKII, Osteoprogenitor markers such as Alp, Opn, Ocn and Bsp in Tony’s sections and other terminology that may require a brief description to provide the readers with a more comprehensive understanding. Overall, this web page is developing well, but there are still many areas for improvement.

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2016 Group Project 3

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{{ANAT2341Project2016header}}
{{Group Assessment Criteria table}}


=Fibroblast Growth Factor Receptor (FGFR) Pathway=
==Introduction==
The Fibroblast Growth Factor (FGF) signalling pathway is critical for regulating progenitor cell proliferation, differentiation, survival and patterning. It is involved in the regulation and development of the early embryo, and is considered to be critical for normal organ, vascular and skeletal development. Furthermore, this pathway is also involved in maintaining adult tissues through the regulation of metabolic functions and tissue repair (which is often through the reactivation of the same signalling pathways involved in early development.) <ref><pubmed>25772309</pubmed>[http://www.ncbi.nlm.nih.gov/pubmed/25772309]</ref>

==History==
Fibroblast growth factor (FGF) was initially discovered in pituitary extracts through experiments conducted in 1973. Researchers had noticed the growth stimulating effects that these isolated factors had, in that they induced fibroblast proliferation. Due to their ability to stimulate fibroblast proliferation they were termed "FGFs". Today, a variety of subtypes of FGFs have been discovered and categorised into a large family that exist in organisms including humans as well as nematodes. In addition, it was soon discovered that not all FGFs can stimulate fibroblasts.

(add timeline)

== Overview Of The FGFR Pathway==
22 protein families of have been identified from the FGF signalling pathway, 18 of which are secreted signalling proteins (FGF1-10, and FGF16-23) that interact with 4 tyrosine kinase FGF Receptors (FGFR1-4) and the other 4 are intracellular non-signalling proteins (iFGFs; FGF11-14).
<ref><pubmed>25772309</pubmed>[http://www.ncbi.nlm.nih.gov/pubmed/25772309]</ref>

FGFRs are comprised of 3 immunoglobulin domains (IgI-III), with IgIII being the closest to the transmembrane, and IgI being the furthest away. As shown in the image, an acidic box (AD) is located in-between IgI and IgII, IgII contains a heparin-binding domain (HBD), which is important in signal transduction, and IgIII is a transmembrane structure with kinase and interkinase domains (KD and IKD) within the intracellular space. <ref><pubmed>16216232</pubmed>[http://www.ncbi.nlm.nih.gov/pubmed/16216232]</ref>

===Signal Transduction===
FGF ligands linked to heparin sulfate proteoglycan (HSPG) bind to both the IgII and IgIII domain of the receptor (with the heparin component specifically binding to IgII) resulting in dimerisation of the receptors and activation of signal transduction pathways through the phosphorylation of tyrosine residues. <ref><pubmed>16216232</pubmed>[http://www.ncbi.nlm.nih.gov/pubmed/16216232]</ref>

''- Different transduction pathways it has''

''- Add image''

==Role In Embryonic Development==

===Patterning Of The Embryonic Axis===
In the process of patterning of the embryonic axis, the caudal primordium that is part of the neural plate, contains cells that are rapidly dividing and is able to maintain itself as a growth region (this region is considered to be of "stem cell" status). The expanding populations of dividing cells us spread along the neural tube by cell movements of convergence and extension. In the process by which cells are driven out of the tube, they change their pattern of movement which eventually causes a gradual restriction in space<ref><pubmed>8575335</pubmed></ref>. Within this process, it is the misexpression of a dominant negative FGFR construct in the tissue which causes these cells prematurely to leave the stem cell region and to change their movement patters as if they had aged<ref><pubmed>11389440</pubmed></ref>.

Furthermore, Mathias et al. (2001) suggest that FGFR is required in order to maintain this stem cell status in the caudal neural plate during patterning of the nervous system. In addition, it is possible that FGF serves the purpose of acting as a caudalizing factor for the neural tube because it is capable of prolonging the window of time during which cells are exposed to a caudalizing factor.

In summary, FGF signalling is important in regulating the maturation of developing cells which are gradually being laid down in a caudal direction along the axis of the neural tube.
 
===Induction/Maintenance Of Mesoderm And Neuroectoderm===

===Organogenesis===
====Limb Bud====
Limb buds which are comprised of lateral plate mesoderm (LPM) cells and an overlying surface ectoderm, are formed roughly week 4 of embryonic development as a result of interactions between the mesoderm and ectoderm germ layers. FGF signaling (along with its interactions with other signaling pathways) is critical for the initiation and proximal-distal growth of limbs from a limb bud structure.<ref><pubmed>9620845</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/9620845]</ref> Prior to bud formation, FGF10 is widely expressed in the LPM and is stabilized by the WNT signaling proteins. ('''''REF''''') FGF10 is responsible for stimulating the expression WNT3 (and downstream transcription factors including SP6 and SP8)<ref><pubmed>15358670</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/15358670]</ref> in the overlying ectoderm, which results in the formation of the Apical Ectodermal Ridge (AER), a specialised thickening of epithelium located towards the proximal end of the bud that is required for growth,<ref><pubmed>25772309</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/25772309]</ref> and subsequently stimulate FGF8. FGF8 is responsible for continued growth of the underlying mesoderm (''keeping in mitotically active state?'') and positive feedbacks on FGF10 (stimulating increased FGF8 expression). FGF8 is the known AER-specific FGF to be expressed throughout, although other FGFs are expressed in the posterior of the AER (including Fgf4, Fgf9 and Fgf17) and are thought to have supporting roles.<ref><pubmed>11101846</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/11101846]</ref><ref><pubmed>12152071</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/12152071]</ref>
FGFs in the AER signal FGFR1 and FGR2 in distal mesenchyme, activating ETV1 and EWSR1 which function to help to maintain Fgf10 expression.<ref><pubmed>25109552</pubmed> [http://www.ncbi.nlm.nih.gov/pubmed/25109552]</ref>

''- Zone of polarizing activity (ZPA)''

''- Interaction with SHH''

''- FGF signaling is also involved in lung initiation and development, and has similar underlying process.''

====Kidney/External Genitalia====
 
James

====Inner Ear Development====

==Animal Models==

(jocelyn)

==Abnormalities==

(Kristine)

 
 

==Glossary==
''(Manraaj)''
 
 

==References==

<references/>

==Extra Resources==
Useful review articles that may be worth a read through:

http://onlinelibrary.wiley.com/doi/10.1002/wdev.176/full

http://www.nature.com.wwwproxy0.library.unsw.edu.au/nrd/journal/v8/n3/pdf/nrd2792.pdf

http://www.sciencedirect.com.wwwproxy0.library.unsw.edu.au/science/article/pii/S0012160605006184

http://www.nature.com.wwwproxy0.library.unsw.edu.au/nrm/journal/v14/n3/full/nrm3528.html

http://onlinelibrary.wiley.com.wwwproxy0.library.unsw.edu.au/doi/10.1002/jcp.24649/full

http://genesdev.cshlp.org/content/29/14/1463.full (FGF signalling and skeletogenesis, specifically how mutations to the FGF signalling pathway may be responsible for skeletal diseases)

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Talk:2016 Group Project 3

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{{ANAT2341Project2016discussionheader}}

==Comments by Group 3==
[[User:Z5015686|Z5015686]] ([[User talk:Z5015686|talk]]) 12:36, 19 August 2016 (AEST) I thought looking into how prenatal cannabis exposure influences signalling during development might be interesting

[[User:Z5017002|Z5017002]] ([[User talk:Z5017002|talk]]) 12:47, 19 August 2016 (AEST) Ooh cool idea, I agree that looks really interesting, there seems to be a lot of literature about its influence on brain development

[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]])z5015544[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) Thats excellent, what about the sonic hedgehog pathway?

[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]])Other ideas[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) WNT Signaling Pathway is another one to look at

How can we harvest stem cells from the embyro for use in later life - z5015337

[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]])z5015544[[User:Z5015544|Z5015544]] ([[User talk:Z5015544|talk]]) Ok guys I created a couple of subheadings and provided a brief history. Make sure to use primary research articles that are peer-reviewed because I just spoke to Dr Hill and noticed he stressed that a lot.

[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]]) I have scoured through the projects of old to get a better idea about what is expected from us for this project - [[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]])

[[User:Z5015337|Z5015337]] ([[User talk:Z5015337|talk]])I found this giant slab of text regarding the structures of the receptors involved from a journal article and I am working through culling it down for a usable structure definition: FGF receptors and FGF signal transduction. FGFRs are modular proteins comprising 3 immunoglobulin domains (IgI, IgII and IgIII). IgI and IgII are separated by an acidic box (AD). IgII contains a heparin binding domain (HBD). The IgIII domain is followed by a unique transmembrane (TM), a juxtamembrane (JM) and a kinase domain (KD) interrupted by an interkinase domain (IKD). FGF ligands linked to heparin sulfate proteoglycan (HSPG) bind to IgII and IgIII of FGFR. This results in the dimerization and the subsequent transactivation by phosphorylation of specific tyrosine residues. The main two transduction pathways involve the phospholipase C-γ (PLCγ) and the Ras/MAP kinase. The SH2 domain of the PLCγ interacts with the phosphorylated Y766 of the activated receptor. The activated PLCγ hydrolyzes the phosphatidyl-inositol-4,5-diphosphate (PIP2) to inositol-1,4,5-triphophate (IP3) and the diacylglycerol (DAG). IP3 releases Ca2+ while DAG activates the protein kinase C-δ (PKCδ). Activated PKCδ activates Raf by phosphorylating its S338 and stimulates the downstream pathway in a Ras independent manner. The main pathway involves the interaction of the docking protein FRS2α with the amino-acid residues 407–433 (Xu et al., 1998). This protein is activated by phosphorylation on multiple tyrosine residues and subsequently interacts and activates Grb2 linked to Sos, a nucleotide exchange factor involved in the activation of Ras. Activated Ras then activates Raf which stimulates MEK which in turn phosphorylates the MAP kinase ERK. This last activated component translocates to the nucleus and phosphorylates specific transcription factors of the Ets family which in turn activate expression of specific FGF target genes. P: phosphorylation

Talk:2016 Group Project 3

2016-09-02T09:24:05Z

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This is the version of the picture I would like to be assessed on

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=Effect of extracellular Ca2+ depletion on the human zona pellucida-induced intracellular [Ca2+] increase in spermatozoa=

Capacitated, Fura-2-loaded spermatozoa were incubated in normal BWW medium (upper curve) or in BWW medium lacking calcium (lower curve). One minute before adding hZP, EGTA (500 μM) was added to the Ca2+ free BWW, to ensure that the extracellular medium was devoid of Ca2+. Solubilised hZP (2/μl) was added (arrow) to the medium for each incubation. Results are expressed as the fluorescence excitation ratio (340/380 excitation wavelengths, in arbitrary fluorescence units (AFU)) as a function of time (min). A typical experiment is shown.

==Reference==

<pubmed> PMC1712232 </pubmed>

[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1712232/]

==Copyright==

Copyright © 2006 Patrat et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

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How can we harvest stem cells from the embyro for use in later life - z5015337

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