|Student Information (expand to read)|
Please leave this template on top of your student page as I will add your assessment items here.
Beginning your online work - Working Online in this course
|Lab 1 Assessment - Researching a Topic|
|In the lab I showed you how to find the PubMed reference database and search it using a topic word. Lab 1 assessment will be for you to use this to find a research reference on "fertilization" and write a brief summary of the main finding of the paper.
|Lab 2 Assessment - Uploading an Image|
OK you are now in a group
Initially the topic can be as specific or as broad as you want.
Chicken embryo E-cad and P-cad gastrulation
|Lab 4 Assessment - GIT Quiz|
Design 4 quiz questions based upon gastrointestinal tract. Add the quiz to your own page under Lab 4 assessment and provide a sub-sub-heading on the topic of the quiz.
An example is shown below (open this page in view code or edit mode). Note that it is not just how you ask the question, but also how you explain the correct answer.
|Lab 5 Assessment - Course Review|
|Complete the course review questionnaire and add the fact you have completed to your student page.|
|Lab 6 Assessment - Cleft Lip and Palate|
|Lab 7 Assessment - Muscular Dystrophy|
|Lab 8 Assessment - Quiz|
|A brief quiz was held in the practical class on urogenital development.|
|Lab 9 Assessment - Peer Assessment|
|Lab 10 Assessment - Stem Cells|
|As part of the assessment for this course, you will give a 15 minutes journal club presentation in Lab 10. For this you will in your current student group discuss a recent (published after 2011) original research article (not a review!) on stem cell biology or technology.
|Lab 11 Assessment - Heart Development|
|Read the following recent review article on heart repair and from the reference list identify a cited research article and write a brief summary of the paper's main findings. Then describe how the original research result was used in the review article.
Week 1 Homework
I studied the Belbin Team Roles in a previous course and identified myself as a Teamworker, which I still definitely agree with, but I'd probably also add that I have the tendencies of a Complete Finisher. In group assignments I always prefer not to take charge and rather to provide support by facilitating discussions and encouraging good communication within the group. In the past, I've often mediated between my real life friends when conflict happens so I'm comfortable in doing that for any group situation I find myself in. I'm also very indecisive as a person and I know this reflects into any group work that I do because I find it difficult if I have to lead or make choices for the rest of the team. I would also say that because I don't particularly look forward to group assignments in the first place, because I'd much rather complete a task by myself, I can sometimes be a Complete Finisher. I know that I hesitate having to rely on other people because I worry that they won't do something the way I would have chosen to do it.
Lecture 1: Fertilisation (2/8/16)
I've always found fertilisation to be an exciting and interesting topic. Even though I've studied it before in previous courses I still find it so fascinating just how much goes into the 'simple' union of a sperm and an egg cell. The way that so many processes and reactions and biological design come together to allow fertilisation to happen really amazes me. But I think the most interesting thing I heard in today's lecture was about the zona pellucida and the ZP2 protein, and how it's used as a signal to attract the sperm to bind to the ovum, and then modified to prevent polyspermy by stopping additional sperm from binding. I'd never learnt about this before so it was really interesting to understand the mechanism involved.
|Mark Hill (talk) 12:36, 5 August 2016 (AEST) Very good. maybe a little to many sub-sub-sub- headings, this will get messy. I will discuss in today's lab online formatting etc.|
Lab 1 Assessment
IVF culture medium affects post-natal weight in humans during the first 2 years of life.
Sander H.M. Kleijkers, Aafke P.A. van Montfoort, Luc J.M. Smits, Wolfgang Viechtbauer, Tessa J. Roseboom, Ewka C.M. Nelissen, Edith Coonen, Josien G. Derhaag, Lobke Bastings, Inge E.L. Schreurs, Johannes L.H. Evers & John C.M. Dumoulin
- In this study, Kleijkers et al. investigated the relationship between the culture media used for embryos during the process of IVF and the subsequent development of the IVF children in early life. This followed on from previous research in which it was observed that the choice of culture medium had an impact on birthweight as well as development of the fetus during pregnancy. 1432 IVF treatments were initially involved and each was randomly allocated to either grow in Cook medium or Vitrolife medium. From this, 126 embryos from the Cook group and 168 embryos from the Vitrolife group were successfully birthed and used for further study. Kleijkers et al. contacted all of the parents two years after the initial birth for records of the postnatal weight, height, and head circumference of their child over the two year period. Statistical analysis and different analytical models were used to compare the collected data. It was observed that the weight of singletons whose embryos had been cultured in Cook medium was consistently lower than that of the Vitrolife group; this confirms that the effect of culture media on fetal growth, as had been previously researched, persists in early postnatal development. Kleijkers et al. propose that these results show the sensitivity of the human embryo to its environment, whether in vivo or in vitro. Hence because the chosen media for the embryo is the environment it grows in before implantation, the adaptation of this embryo to the media, possibly by epigenetic modification, is seen to have consequences for later development. This emphasises the need for further research into the growth media used for IVF treatment to ensure an optimal environment for the preimplantation growth of the embryo, and therefore both prenatal and postnatal development of an IVF child.
|Mark Hill 18 August 2016 - You have added the citation correctly and written a good brief summary of the article findings. You also seem to have practiced using some of the Wiki formatting tools. So the very conditions of initial growth may have long-term developmental ramifications. You can see why research in this area is important. These days we have a reasonably large IVF cohort to begin to get some useful data.||Assessment 5/5|
Lab 2 Assessment
Human blastocyst attached to decidualized human endometrial stromal cells after 72 hours of co-culture.
|Mark Hill 29 August 2016 - All information Reference, Copyright and Student Image template correctly included with the file and referenced on your page here.||Assessment 5/5|
Lab 3 Assessment
|Mark Hill 31 August 2016 - Lab 3 Assessment Quiz - Mesoderm and Ectoderm development. All correct, well done!||Assessment 5/5|
Lab 4 Assessment
Gastrointestinal Development Quiz
|Mark Hill 17 October 2016 - GIT Quiz covers a range of related topics. Question 1 identifies difference between endoderm and mesoderm origins. Question 2 is about blood supply, not a testing question as the 3 options are given in several options. Question 3 and 4 are good testing questions.||Assessment 5/5|
Lab 5 Assessment
I completed the course review questionnaire!
|Mark Hill 17 October 2016 - course review questionnaire.||Assessment 5/5|
Lab 6 Assessment
Meta-analysis Reveals Genome-Wide Significance at 15q13 for Nonsyndromic Clefting of Both the Lip and the Palate, and Functional Analyses Implicate GREM1 As a Plausible Causative Gene.
Kerstin U Ludwig, Syeda Tasnim Ahmed, Anne C Böhmer, Nasim Bahram Sangani, Sheryil Varghese, Johanna Klamt, Hannah Schuenke, Pinar Gültepe, Andrea Hofmann, Michele Rubini, Khalid Ahmed Aldhorae, Regine P Steegers-Theunissen, Augusto Rojas-Martinez, Rudolf Reiter, Guntram Borck, Michael Knapp, Mitsushiro Nakatomi, Daniel Graf, Elisabeth Mangold & Heiko Peters
- In their research, Ludwig et al. looked at findings from previous studies and confirmed that the 15q13 region is a risk locus for developing nonsyndromic cleft lip and palate (nsCL/P) but not nonsyndromic cleft lip only (nsCLO). By experimenting on mice, they also associated genetic variation in a 5 kb region downstream from the Gremlin-1 (Grem1) transcription start site with developing nsCL/P. They observed localised expression of Grem1 in the soft palate and in the processes forming the lip during mouse embryogenesis. While Grem1-deficient mice did not develop lip or palate defects, the addition of ectopic Grem1 was shown to have a pathogenic effect on the morphogenesis of the palatal shelves during secondary palate development. Grem1 is known to be critical for limb bud development, but not lip and palate development. Its role in limb bud development is to establish a positive feedback loop between Shh and Fgf via inhibition of Bmp signalling (a negative regulator of SHH expression in limb mesenchyme). However, previous research determined that Bmp signalling is a positive regulator of Shh expression in the palatal shelf epithelium and cell proliferation in the anterior palatal shelf mesenchyme. Bmp4 and Bmp2 are involved in the normal development of the anterior palate and Bmp4 and Bmp7 are expressed in the posterior palatal shelves. Therefore, it was concluded that an abnormality in Grem1 expression could interrupt normal development of the secondary palate due to the inhibition of Bmp signalling.
|Mark Hill 17 October 2016 - GREM1 is a novel factor and your summary is useful and you have good to also included the signaling pathway involved.||Assessment 5/5|
Lab 7 Assessment
Duchenne muscular dystrophy (DMD) is the most common muscular dystrophy, affecting 1 in 3,500-5,000 newborn males globally. It is caused by recessive loss-of-function mutations in the dystrophin gene on the X chromosome. Frame-shift mutations in the gene lead to failed expression of the dystrophin mutation and hence the manifestation of DMD. One-third of DMD cases can occur by spontaneous mutation, meaning that a positive family history is not required for diagnosis. Physical examinations, molecular biopsies, genetic testing, and review of clinical history are all involved when diagnosing DMD. Serum creatine kinase (CK) is used as an initial diagnostic tool to measure the levels of muscle enzymes. DMD is defined at the molecular level as producing no dystrophin and clinically as the loss of ambulation at 12 years of age or younger. A less severe mutation of the dystrophin gene, such as an in-frame deletion, can instead produce a truncated version of the protein which results in Becker muscular dystrophy (BMD), a milder form of DMD.
Dystrophin is a major muscle protein which connects the cytoskeleton (cytoskeletal actin, microtubules, and intermediate filaments) and the extracellular matrix (ECM). Dystrophin is anchored to the plasma membrane by phospholipids and β-dystroglycan. The dystrophin complex is found in costameres of skeletal and heart muscle, which are located at the periphery of the muscle fibers. Costameres are involved in transmitting forces from the cytosol to the ECM and therefore prevent the collapse of the cell membrane during muscle contraction. Hence, in DMD and BMD the impaired function of dystrophin results in frequent cell damage when the muscle contracts. The rupture of the plasma membrane causes leakage of the intracellular components; for example, creatine kinase can be released from the damaged cell which explains the high concentrations of serum creatine kinase in DMD patients.
The most common mutation implicated in DMD and BMD is a deletion of one or more exons, accounting for 60-70% of DMD cases and 80-85% of BMD cases. Point mutations are have been found in approxiamtely 26% of DMD cases and 13% of BMD cases, while exonic duplications are involved in 10-15% of DMD cases and 5-10% of BMD cases. Other possible mutations include subexonic insertions, deletions, splice mutations, and missense mutations.
Animal models used to investigate DMD and BMD include the mdx mouse and the grmd dog. Due to the size of the dystrophin gene, it is difficult to treat DMD or BMD with gene therapy. The idea of producing a smaller version of the protein, micro-dystrophin, has been attempted, but due to its smaller size it cannot act as a perfect functional substitute for dystrophin. In the case of DMD, exon skipping therapy has been investigated as a way of altering the mutation of the dystrophin gene. Instead of the frame-shift mutation which results in no functional dystrophin being produced, the splicing of the mRNA can be modified to exclude one or more additional exons which therefore restores the reading frame and results in production of a BMD-like dystrophin (truncated, but still partly functional). This has been accomplished by introducing small antisense oligonucleotides (AONs) sequences, which bind to exon splice junctions and inhibit the action of the spliceosome. However, this ultimately only lessens the severity of the disease and still presents the problem of treating the BMD-like symptoms. There is still no effective cure for either DMD or BMD. Most available treatments are focused on slowing the progression of the diseases and continued research is being done into ways of converting a severe phenotype of disease to a more mild phenotype.
|Mark Hill 17 October 2016 - You have answered all questions and also included the source references, well done.||Assessment 5/5|
Lab 9 Assessment
These are very good reviews of the project pages, with some specific examples. They include a balanced critical assessment, perhaps a little too on the positive side, given the existing status of some of these pages. 8/10
Group 1 Peer Review
Great job on all the content you’ve produced as a group so far. It’s clear you guys have done a lot of research into the topic and you’ve identified key aspects of Wnt signalling. The information you have is all relevant, everything is referenced, and all your abbreviations are defined. It’s really good that you have included some specific studies and explained the findings and what they discovered about Wnt signalling. It’s great you’ve also started to look into the abnormalities so if you put some more info into that I think it presents a really interesting topic for the reader to read about.
The first things I would point out is mostly for the structure/layout of your page. Make sure you use the correct wiki formatting so the page looks uniform and clean. You should separate your references out from the main body of info and collate them properly at the end of the page. Also make sure that you have in-text referencing so the reader knows exactly where the information is from. And for your content, I think it would look more professional to present it in structured paragraphs instead of bullet points. I would suggest having a proper introduction paragraph so that the reader gets an immediate overview of Wnt signalling and which aspects you’ll be exploring, rather than going straight into explanation of the pathway. Also, while you do have good headings for each section I think putting in more specific subheadings will help both you and the reader to organise the information better. In terms of the info you have so far, I would just make a point that you should try and get most of the content from primary sources instead of review articles. Additionally, because you are focusing on Wnt signalling in skin development I don’t think you have enough explanation in that area. Since it’s your focal aspect then I think you should explore a lot more of the research and the related abnormalities that have been found. You could also just include some links to papers that describe Wnt signalling in other embryonic roles since you aren’t investigating those. Finally I would suggest making the page more interesting by including images, diagrams, tables, timeline, etc. so it’s not just paragraphs of text one after the other (and to fulfill the assessment criteria). But overall you guys have made great progress - I hope these comments will help you improve!
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 4 Peer Review
First off you guys have chosen great headings and subheadings! It’s really helpful in breaking down your information to be better understood and I like all the aspects you’ve chosen to explore. Your content so far is clear and concise and most of it is correctly referenced - well done particularly on the info for animal models. The examples of primary research you’ve included are also a great addition. The information you’ve presented is also written well and in a way that’s not too scientific so it’s easy to understand.
It would be great if you included an introduction paragraph to just give a brief overview of Hedgehog signalling. While your animal model content is good, I think you need a lot more info for human embryonic development (considering that it should be the focus of the project) - you’ve mentioned organogenesis very briefly, but I think if you explored each of the systems in greater detail then it would really improve your page. I would strongly recommend including a glossary as well. Make sure you have captions for your images so the reader understands why the image is relevant to your text. Also you should fully define all the abbreviations somewhere (either in your glossary on the image’s page) for the reader’s benefit. If you have some more images in the signalling/animal model sections I think that would break up the paragraphs a bit more and make it easier to read. And you might want to include a summary table, maybe of the molecular pathway factors, somewhere. But overall you’ve started off really well as a team - keep working hard to finish off/improve each section.
Group 5 Peer Review
Congrats Group 5 on producing a really great looking page so far! Straightaway I like that you have an introduction paragraph and that I can immediately see inclusion of tables, images, and some correct referencing. Explaining the origin of the T-box name is a great piece of background info to include (maybe make it a proper subheading though?). You’ve also touched on some of the history of the gene/signalling pathway in your paragraphs but it might be good to also present that in a brief timeline/table. Your table for T-box family features is really great - especially because of inclusion of main expression sites and the related abnormalities. Also, you have references to primary research articles so it’s good to see you’re backing up your content with accurate and relevant sources. You’ve done a really great job on exploring the animal models as well.
Ultimately you guys have done great work so my suggestions for improving your page are mostly minor! You have a lot of PMID links just left at the end of some paragraphs so make sure you get those properly listed at the end in your reference section. If you change your pictures to thumbnails then I think they would integrate into your text better (because at the moment where they are placed breaks up the text). Also, I’m not sure if there’s a particular reason why you did this in the first place but I wouldn’t capitalise all the subheadings in the abnormalities section. And I suggest moving the ‘Ancient origins and evolution of the T-box gene family’ near the top of your page, because at the moment it seems out of place and doesn’t really flow on from discussing the abnormalities. The other thing I would say is that - if it’s possible - it would be great if you could explain more about the actual molecular pathway and include a picture of the molecules/factors involved, because at the moment you’ve only described it in the context of different TBX genes being expressed in each developmental role. I think especially if you have an image of the structure of some of the different proteins, transcription factors, etc. then it would really help to visualise the molecular aspects of the pathway. Hope my comments are helpful!
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!
|Lab 10 - Stem Cell Presentations 2016|
|Group Mark||Assessor General Comments|
Group 1: 15/20
Group 2: 19/20
Group 3: 20/20
Group 4: 19/20
Group 5: 16/20
Group 6: 16/20
|The students put great effort in their presentation and we heard a nice variety of studies in stem cell biology and regenerative medicine today. The interaction after the presentation was great.
As general feedback I would like to advise students to:
Lab 11 Assessment
Distinct phases of cardiomyocyte differentiation regulate growth of the zebrafish heart.
Emma de Pater, Linda Clijsters, Sara R. Marques, Yi-Fan Lin, Zayra V. Garavito-Aguilar, Deborah Yelon & Jeroen Bakkers
- In this study, de Pater et al. investigated the regulation of development of the zebrafish heart. Although the process of heart development (e.g. elongation, septation, heart looping) of vertebrates is well known, the regulatory mechanisms are less understood. De Pater et al. performed their research with the aim of looking into cardiomyocyte differentiation during cardiac development. By counting the number of differentiated cardiomyocytes of the linear zebrafish heart tube vs. the looped chambers, they found that the cardiomyocytes in the heart tube were increased during the process of looping. They also stained cells with BrdU to detect proliferating cells, then used protein expression detection and a timing assay to discover that there were distinct phases of proliferation and differentiation among different cell populations. It was seen that cardiomyocyte differentiation began in the ventricle and continued along the atrium, which also allowed new cardiomyocytes to be added at the venous pole of the heart tube. De Pater et al. also observed a subsequent second phase of differentiation located at the arterial pole. In conclusion, the first phase of differentiation (which produced the cardiomyocytes that formed the ventricle and atrium) was completely separate from the second phase (addition of cells to the arterial pole). They also found that different signalling mechanisms were involved in the different phases. Therefore the temporal regulation and the signalling regulation of the phases of differentiation at each pole were different.
- This research was referred to in the 2016 review article, 'Building and re-building the heart by cardiomyocyte proliferation', by Foglia & Poss. De Pater et al.'s findings were mentioned as evidence for cardiac growth in zebrafish occurring specifically through the proliferation of existing cardiomyocytes.