|Embryology - 20 May 2019 Expand to Translate|
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- 1 Introduction
- 2 Some Recent Findings
- 3 Apoptosis
- 4 Axes
- 5 Cellular Mechanisms
- 6 Cell Migration
- 7 Adhesion
- 8 Molecular Mechanisms
- 9 Model Differences
- 10 References
- 11 External Links
- 12 Glossary Links
These notes are intended to introduce a number of different mechanisms at the all levels that form structures within the embryo. These are general notes about these mechanisms giving only a few examples. For specific tissues and organs read the system notes. What is remarkable, given our biological diversity, is the strong evolutionary conservation of these developmental mechanisms. Researchers should still recognise that there still exist significant differences between "animal models" and human development.
|Molecular Links: molecular | genetics | epigenetics | mitosis | meiosis | X Inactivation | Signaling | Factors | Mouse Knockout | microRNA | Mechanisms | Developmental Enhancers | Protein | Genetic Abnormal | Category:Molecular|
|Factor Links: AMH | hCG | BMP | sonic hedgehog | bHLH | HOX | FGF | FOX | Hippo | LIM | Nanog | NGF | Nodal | Notch | PAX | retinoic acid | SIX | Slit2/Robo1 | SOX | TBX | TGF-beta | VEGF | WNT | Category:Molecular|
Some Recent Findings
|More recent papers|
This table allows an automated computer search of the external PubMed database using the listed "Search term" text link.
|These papers originally appeared in the Some Recent Findings table, but as that list grew in length have now been shuffled down to this collapsible table.
|This single term "apoptosis" describes the way in which the majority of cells die within our adult body are removed every day, "Programmed Cell Death". In development, apoptosis begins in the early blastocyst and is a developmental mechanism found throughout tissues in the embryo and fetus developmental stages. In addition to the many developmental roles this process is used in multicellular organisms to remove cells that are: aged, superfluous, infected, contain genetic errors or are transformed.||
Neuron apoptosis or necrosis (EM).
All embryos occupy 3 D space and appear differently externally and internally within this space. This gives us 3 different axes which need to be determined: Head/Tail (rostro/caudal), Front/Back (anterior/posterior), and Left/Right. The left/right axis appears at first mirror symetrical, and looks very similar externally, but clearly many internal organs are not duplicated (heart, liver, brain etc).
The left/right axis appears at first mirror symetrical, and looks very similar externally, but clearly many internal organs are not duplicated (heart, liver, brain etc).
Embryo left-right asymmetry pathway
These notes are intended to introduce a number of mechanisms at the cellular level that form structures within the embryo. These cellular dynamic and physical interactions form basic tissue structures of epithelia, connective tissues and features such as tubes.
Neural Crest Migration
Germ Cell Migration
|Migration 1||Migration 2||Migration 3|
Adhesion EM Images
Differential positioning of adherens junctions is associated with initiation of epithelial folding
Nature. 2012 Mar 28. doi: 10.1038/nature10938.
Wang YC, Khan Z, Kaschube M, Wieschaus EF. Source 1] Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA  Howard Hughes Medical Institute, Princeton University, Princeton, New Jersey 08544, USA.
- "During tissue morphogenesis, simple epithelial sheets undergo folding to form complex structures. The prevailing model underlying epithelial folding involves cell shape changes driven by myosin-dependent apical constriction. Here we describe an alternative mechanism that requires differential positioning of adherens junctions controlled by modulation of epithelial apical-basal polarity. Using live embryo imaging, we show that before the initiation of dorsal transverse folds during Drosophila gastrulation, adherens junctions shift basally in the initiating cells, but maintain their original subapical positioning in the neighbouring cells. Junctional positioning in the dorsal epithelium depends on the polarity proteins Bazooka and Par-1. In particular, the basal shift that occurs in the initiating cells is associated with a progressive decrease in Par-1 levels. We show that uniform reduction of the activity of Bazooka or Par-1 results in uniform apical or lateral positioning of junctions and in each case dorsal fold initiation is abolished. In addition, an increase in the Bazooka/Par-1 ratio causes formation of ectopic dorsal folds. The basal shift of junctions not only alters the apical shape of the initiating cells, but also forces the lateral membrane of the adjacent cells to bend towards the initiating cells, thereby facilitating tissue deformation. Our data thus establish a direct link between modification of epithelial polarity and initiation of epithelial folding."
Role of the gut endoderm in relaying left-right patterning in mice
PLoS Biol. 2012 Mar;10(3):e1001276. Epub 2012 Mar 6. Viotti M, Niu L, Shi SH, Hadjantonakis AK. Source Developmental Biology Program, Sloan-Kettering Institute, New York, New York, United States of America.
- "Establishment of left-right (LR) asymmetry occurs after gastrulation commences and utilizes a conserved cascade of events. In the mouse, LR symmetry is broken at a midline structure, the node, and involves signal relay to the lateral plate, where it results in asymmetric organ morphogenesis. How information transmits from the node to the distantly situated lateral plate remains unclear. Noting that embryos lacking Sox17 exhibit defects in both gut endoderm formation and LR patterning, we investigated a potential connection between these two processes. We observed an endoderm-specific absence of the critical gap junction component, Connexin43 (Cx43), in Sox17 mutants. Iontophoretic dye injection experiments revealed planar gap junction coupling across the gut endoderm in wild-type but not Sox17 mutant embryos. They also revealed uncoupling of left and right sides of the gut endoderm in an isolated domain of gap junction intercellular communication at the midline, which in principle could function as a barrier to communication between the left and right sides of the embryo. The role for gap junction communication in LR patterning was confirmed by pharmacological inhibition, which molecularly recapitulated the mutant phenotype. Collectively, our data demonstrate that Cx43-mediated communication across gap junctions within the gut endoderm serves as a mechanism for information relay between node and lateral plate in a process that is critical for the establishment of LR asymmetry in mice."
This page is a link to many different resources related to Molecular Development. In current years we have turned from wanting to merely describe the events of embryogenesis, to a desire to understand the mechanisms of development. This has been a boon in allowing the use of many (easier) model systems such as the genetist's tool the fruitfly, and the worm, frog, chicken, zebrafish and mouse (see other embryos page).
A continuing theme also seems to be the reuse of signals at different times and places within the embryo, for diiferent jobs. This has given rise to the concept of "switches" which by themselves may contain no "information" but to activate other genes or switches. Finally, you can imagine that of our 20,000-25,000 protein-coding genes, a large number of these may only be expressed during development or if reused, have a completely different role in the mature animal.
Eukaryotic organisms reproduce by generating haploid gamete cells, oocytes and spermatozoa, that in fertilization recombine to form the first diploid cell of the new organism. In normal human development, each gamete contains a single sex chromosome, the oocyte carries an X chromosome and the spermatozoa carries either an X or a Y chromosome. Initial sex determination is therefore determined by the spermatozoa and the specific sex chromosome it contains.
In development, the term sex determination used to apply more broadly to how the Y chromosome determined male development. It was thought that female sex determination was the "default mechanism", but we now know that there are also female specific mechanisms.
- Links: genital
Epigenetics, as the name implies, is the inheritance mechanisms that lie outside the DNA sequence of our genome and genes. These molecular mechanisms include: DNA methylation, histone modification, and those related to the microRNA machinery.
- Links: epigenetics
While many mechanisms of development are strongly conserved, researchers should still recognise that there still exist significant differences between "animal models" and human development.
A few examples:
- respiratory development in human and mouse
- Template:X inactivation - ZFX on the X chromosome in humans escapes X inactivation while in mouse it is inactivated.
- Waldner C, Roose M & Ryffel GU. (2009). Red fluorescent Xenopus laevis: a new tool for grafting analysis. BMC Dev. Biol. , 9, 37. PMID: 19549299 DOI.
- Ebisuya M & Briscoe J. (2018). What does time mean in development?. Development , 145, . PMID: 29945985 DOI.
- Inomata H. (2017). Scaling of pattern formations and morphogen gradients. Dev. Growth Differ. , 59, 41-51. PMID: 28097650 DOI.
- Nance J. (2014). Getting to know your neighbor: cell polarization in early embryos. J. Cell Biol. , 206, 823-32. PMID: 25267293 DOI.
- Harding MJ, McGraw HF & Nechiporuk A. (2014). The roles and regulation of multicellular rosette structures during morphogenesis. Development , 141, 2549-58. PMID: 24961796 DOI.
- Ueda H, Fujita R, Yoshida A, Matsunaga H & Ueda M. (2007). Identification of prothymosin-alpha1, the necrosis-apoptosis switch molecule in cortical neuronal cultures. J. Cell Biol. , 176, 853-62. PMID: 17353361 DOI.
- Norris DP. (2012). Cilia, calcium and the basis of left-right asymmetry. BMC Biol. , 10, 102. PMID: 23256866 DOI.
- Nikolić MZ, Sun D & Rawlins EL. (2018). Human lung development: recent progress and new challenges. Development , 145, . PMID: 30111617 DOI.
- Adler DA, Bressler SL, Chapman VM, Page DC & Disteche CM. (1991). Inactivation of the Zfx gene on the mouse X chromosome. Proc. Natl. Acad. Sci. U.S.A. , 88, 4592-5. PMID: 2052543
Search PubMed: Developmental Mechanisms
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Cite this page: Hill, M.A. (2019, May 20) Embryology Developmental Mechanisms. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Developmental_Mechanisms
- © Dr Mark Hill 2019, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G