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Axis formation:
Axis formation is the determining of the different portions of the embryo that is detrimental in the developmental process because without this axis formation the embryo would not be successful. Genes are the establishers and determinants of axis formation. There are multiple different mechanisms utilized to control these gene gradients. From gap junction communication, movement of cytoplasm to move a gene to one side of the embryo, activating and inhibiting proteins, and Henson’s node in the case of the chicken.[1][2] [3] For the simplest explanation of how these are created and maintained is that specific genes are expressed in certain parts of the embryo and usually inhibit the opposite sides expression to maintain these genetic gradients.
Anterior/Posterior formation:
In chicken axis formation Dorsal and Ventral formation is closely related to Anterior and Posterior due to the disc embryo design that causes much overlap in these two cycles.[2][3] The original step in these two axis formations is the centrifugation of the egg as it travels down the reproductive tract.[3] This causes the proteins to be moved to appropriate locations in the embryo. The Posterior end of the embryo is highly expressed with BMP and B-Catenin coming from the PMZ in the vegetal pole of the embryo establishing the organizer.[2] [3] The next steps in anterior and posterior axis formation can be broken down into three steps.[3]
First, in Chicken embryos, there is the use of Hensen’s node, which is their organizer.[3] Hensen’s node is in high concentration of anterior expression gene noggin.[3] Hensen’s node begins at the most anterior part of the embryo and then moves down the notochord of the embryo to the posterior end of the embryo while, establishing the head and somites as it moves down as well as leaving behind a trail of gene expression.[2][3] These gene gradients that are established are detrimental in creation of axis formation.
The next step in anterior/posterior formation is when Smad1 comes in by upregulation through BMP binding BMPR1 and BMPR2 and then creates Smad1.[3] While this is happening, BMP is being repressed by Noggin while Noggin is repressing BMP, with Noggin being highly expressed in the anterior and BMP being highly expressed in the posterior.[3] While they both inhibit each other from being expressed on the wrong side.[3]
In the final step of Anterior and Posterior axis formation a signaling pathway is creating concentration gradients that have RA and FGF4 both expressing posterior strongly.[1][3] While cryp26 is the prominent anterior gene.[1][3]
Left/Right axis formation:
In left and right axis formation of chick embryos there is a movement of proteins by cell gap junctions that signal for an intercellular current.[1] This moves PitX2 to the left as well as Cerberus and Nodal that establish the heart and gut folds.[3] While, FGF8 is found to be the determinate of the right side because it suppresses all three of the left side proteins.[1] [3]
- ^ a b c d e Schlange, Thomas; Arnold, Hans-Henning; Brand, Thomas (July 2002). "BMP2 is a positive regulator of Nodal signaling during left-right axis formation in the chicken embryo". Development (Cambridge, England). 129 (14): 3421–3429. ISSN 0950-1991. PMID 12091312.
- ^ a b c d Grieshammer, U.; Minowada, G.; Pisenti, J. M.; Abbott, U. K.; Martin, G. R. (December 1996). "The chick limbless mutation causes abnormalities in limb bud dorsal-ventral patterning: implications for the mechanism of apical ridge formation". Development (Cambridge, England). 122 (12): 3851–3861. ISSN 0950-1991. PMID 9012506.
- ^ a b c d e f g h i j k l m n o 1949-, Slack, J. M. W. (Jonathan Michael Wyndham), (2013). Essential developmental biology (3rd ed ed.). Chichester, West Sussex: Wiley. ISBN 9780470923511. OCLC 785558800.
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