How cell movements are coordinated during
morphogenesis is not well understood. We focus on epiboly, which describes the thinning and spreading of a multilayered cell sheet. The first phase of epiboly involves the doming of the yolk
cell up into the overlying blastoderm. We previously showed that over-expression of a dominant– negative eomesodermin a construct inhibits doming. Here I report my analysis of embryos lacking both maternal and zygotic Eomesodermin A (MZeomesa). eomesafh105 mutant embryos (1) exhibit a doming delay, (2) have defective yolk cell microtubules, (3) have tightly packed deep cells with more bleb – like protrusions and (4) express early endoderm markers abnormally.
Despite these phenotypes, the majority of MZeomesa embryos are able to complete epiboly and form endodermal derivatives. In both Xenopus and mice, Eomesodermin has also been implicated in the regulation of gastrulation movements and cell fate specification, suggesting a
conserved role for Eomesodermin throughout vertebrate development.
| Identifer | oai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/25558 |
| Date | 31 December 2010 |
| Creators | Du, Susan |
| Contributors | Bruce, Ashley |
| Source Sets | University of Toronto |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
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