WAVE2 deficiency reveals distinct roles in embryogenesis and Rac-mediated actin-based motility
Copyright policy )WAVE2 deficiency reveals distinct roles in embryogenesis and Rac-mediated actin-based motility
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.
- Boston Children's Hospital United States
- Harvard University United States
- Howard Hughes Medical Institute United States
Mice, Knockout, Stem Cells, Microfilament Proteins, Fibroblasts, Embryo, Mammalian, Actins, Cell Line, Wiskott-Aldrich Syndrome, Wiskott-Aldrich Syndrome Protein Family, rac GTP-Binding Proteins, Mice, Biopolymers, Cell Movement, Mutation, Animals, Protein Isoforms, RNA, Pseudopodia, Cytoskeleton, Gene Deletion
Mice, Knockout, Stem Cells, Microfilament Proteins, Fibroblasts, Embryo, Mammalian, Actins, Cell Line, Wiskott-Aldrich Syndrome, Wiskott-Aldrich Syndrome Protein Family, rac GTP-Binding Proteins, Mice, Biopolymers, Cell Movement, Mutation, Animals, Protein Isoforms, RNA, Pseudopodia, Cytoskeleton, Gene Deletion
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