WAVE2 deficiency reveals distinct roles in embryogenesis and Rac-mediated actin-based motility.
EMBO J
; 22(14): 3602-12, 2003 Jul 15.
Article
in En
| MEDLINE
| ID: mdl-12853475
ABSTRACT
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.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Cell Movement
/
Actins
/
Rac GTP-Binding Proteins
/
Embryo, Mammalian
/
Microfilament Proteins
Limits:
Animals
Language:
En
Journal:
EMBO J
Year:
2003
Document type:
Article
Affiliation country:
United States