Developmental Mechanisms
Contents |
Introduction
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.
- Mechanism Links: Epithelial Invagination | Epithelial Mesenchymal Transition | Epithelial Mesenchymal Interaction | Morphodynamics | Tube Formation | Apoptosis | Molecular
- Molecular Links: Introduction | Genetics | Epigenetics | Mitosis | Meiosis | X Inactivation | Signaling | Factors | Mouse Knockout | microRNA | Mechanisms | Protein | Genetic Abnormal | Category:Molecular
- Factor Links: Sonic hedgehog | Homeobox | FGF | Nanog | Notch | Pax | Retinoic acid | Sox | Tbx | TGF-beta | Wnt | BMP | hCG
Apoptosis
| 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).[1] |
Axes
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).
Cellular Mechanisms
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.
Cell Migration
Neural Crest Migration
|
|
|
|
|
|
|
|
| Cranial Migration |
Germ Cell Migration
|
|
|
| Migration 1 | Migration 2 | Migration 3 |
Adhesion
- Adhesion EM Images: GIT epithelia EM1 | GIT epithelia EM2 | GIT epithelia EM3 | Desmosome EM
- Adhesion Cartoons: Tight junction | Adherens Junction | Desmosome | Gap Junction
Adhesion Cartoons
Tight junction
Adherens Junction
Desmosome
Gap Junction
Adhesion EM Images
GIT epithelia EM1
GIT epithelia EM2
GIT epithelia EM3
Desmosome EM
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 [2] Howard Hughes Medical Institute, Princeton University, Princeton, New Jersey 08544, USA.
Abstract
- "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.
Abstract
- "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."
Molecular Mechanisms
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.
Sex Determination
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 System Development
Epigenetics
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
References
- ↑ Hiroshi Ueda, Ryousuke Fujita, Akira Yoshida, Hayato Matsunaga, Mutsumi Ueda Identification of prothymosin-alpha1, the necrosis-apoptosis switch molecule in cortical neuronal cultures. J. Cell Biol.: 2007, 176(6);853-62 PMID:17353361 | PMC2064059 | J Cell Biol.
Journals
Reviews
Search PubMed
Search PubMed: Developmental Mechanisms
External Links
External Links Notice - The dynamic nature of the internet may mean that some of these listed links may no longer function. If the link no longer works search the web with the link text or name.
- Mechanism Links: Epithelial Invagination | Epithelial Mesenchymal Transition | Epithelial Mesenchymal Interaction | Morphodynamics | Tube Formation | Apoptosis | Molecular
Glossary Links
- 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 | Numbers | Symbols
- Dr Mark Hill 2013, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G
