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Control of cortical actin assembly and cadherin‐catenin localization by GPCRs and RhoGTPases
Author(s) -
Jimenez-Dalmaroni Maximiliano Javier,
Heasman Janet,
Wylie Christopher
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.769.3
Subject(s) - microbiology and biotechnology , biology , cadherin , catenin , xenopus , embryonic stem cell , g protein coupled receptor , actin , actin cytoskeleton , neuroscience , cytoskeleton , wnt signaling pathway , cell , signal transduction , genetics , gene
Many common and permanently disabling human birth defects, such as spina bifida, are caused by the loss of cell shape changes and tissue movements in the early embryo. Therefore, it is important to understand how these cell shape changes are regulated during embryonic development. It has been previously shown that the actin cytoskeleton is required for normal tissue movements at these stages. Furthermore, the expression and localization of cadherin‐catenin complex are relevant for cell adhesion and F‐actin assembly and their lost can increase risk of metastasis in carcinomas and alter normal cell movements during embryonic development. Using the Xenopus laevis embryo and human embryonic stem cells as models, we are currently investigating the mechanisms by which cortical actin assembly is regulated during development and the signaling pathways relevant for the cadherin‐catenin localization. We have identified two G‐protein couple receptors, a novel GPCR receptor termed xFlop and xLPA, and the small GTPase Rac1, as key molecules involved in this process. We hope this research could lead us to not only better understanding of cortical actin assembly and remodeling in early stages of Xenopus laevis embryos and humans, but also to develop novel treatments for spina bifida and human cancer metastasis.