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O2. The antagonism between Sox3 and Snail control cell movements to define the ectodermal/mesendodermal boundary in vertebrates

AutorAcloque, Hervé; Ocaña, Oscar H.; Nieto, M. Ángela
Fecha de publicaciónnov-2010
EditorElsevier
CitaciónDifferentiation 80(S1): S6 (2010)
ResumenWith the exception of the ectodermal derivatives (central nervous system and epidermis), adult tissues and organs are the final product of one or several rounds of epithelial to mesenchymal transitions (EMT) and the reverse process (mesenchymal to epithelial transition or MET) (Thiery et al., 2009). In the embryo itself, the first EMT event occurs at gastrulation. Cells from the single epithelial cell layer (epiblast or primitive ectoderm) move to the midline to form the primitive streak, a linear structure that bisects the embryo along the antero-posterior axis. These are the cells that undergo EMT and internalize to generate the mesoderm and the endoderm, highlighting the importance of the EMT for embryonic development, but also pointing to the need for an EMT repressor in those cells that remain in the ectoderm to become central nervous system and epidermis. Among the key evolutionary conserved factors that induce EMT at gastrulation and at additional developmental processes are the members of the Snail family (Barrallo-Gimeno and Nieto, 2009). However, they need to be downregulated in the adult, as their pathological activation leads to several prominent pathologies including tumour progression and fibrosis (Thiery et al., 2009). Therefore, it is important to identify not only those factors that induce Snail expression but also those that prevent it. These repressors are the candidates to play an important role in protecting cells from undergoing EMT to ensure the formation of ectodermal derivatives during development and to maintain epithelial homeostasis in the adult. I will present data to indicate that Sox3 and Snail factors are mutual repressors that control cells movements to define embryonic territories at gastrulation.
Versión del editorhttps://doi.org/10.1016/j.diff.2010.09.145
URIhttp://hdl.handle.net/10261/167872
DOI10.1016/j.diff.2010.09.145
ISSN0301-4681
E-ISSN1432-0436
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