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WAVE2 deficiency reveals distinct roles in embryogenesis and Rac-mediated actin-based motility.

The EMBO journal | Jul 15, 2003

http://www.ncbi.nlm.nih.gov/pubmed/12853475

The Wiskott-Aldrich syndrome related protein WAVE2 is implicated in the regulation of actin-cytoskeletal reorganization downstream of the small Rho GTPase, Rac. We inactivated the WAVE2 gene by gene-targeted mutation to examine its role in murine development and in actin assembly. WAVE2-deficient embryos survived until approximately embryonic day 12.5 and displayed growth retardation and certain morphological defects, including malformations of the ventricles in the developing brain. WAVE2-deficient embryonic stem cells displayed normal proliferation, whereas WAVE2-deficient embryonic fibroblasts exhibited severe growth defects, as well as defective cell motility in response to PDGF, lamellipodium formation and Rac-mediated actin polymerization. These results imply a non-redundant role for WAVE2 in murine embryogenesis and a critical role for WAVE2 in actin-based processes downstream of Rac that are essential for cell movement.

Pubmed ID: 12853475 RIS Download

Mesh terms: Actins | Animals | Biopolymers | Cell Line | Cell Movement | Cytoskeleton | Embryo, Mammalian | Fibroblasts | Gene Deletion | Mice | Mice, Knockout | Microfilament Proteins | Mutation | Protein Isoforms | Pseudopodia | RNA | Stem Cells | Wiskott-Aldrich Syndrome | Wiskott-Aldrich Syndrome Protein Family | rac GTP-Binding Proteins

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Mouse Genome Informatics (Data, Gene Annotation)

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