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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.

Pubmed ID: 12853475

Authors

  • Yan C
  • Martinez-Quiles N
  • Eden S
  • Shibata T
  • Takeshima F
  • Shinkura R
  • Fujiwara Y
  • Bronson R
  • Snapper SB
  • Kirschner MW
  • Geha R
  • Rosen FS
  • Alt FW

Journal

The EMBO journal

Publication Data

July 15, 2003

Associated Grants

None

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