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Nat Cell Biol. 2001 Oct;3(10):897-904.

N-WASP deficiency reveals distinct pathways for cell surface projections and microbial actin-based motility.

Author information

1
Center for Blood Research, 200 Longwood Avenue, Boston, Massachusetts 02115, USA. ssnapper@hms.harvard.edu

Abstract

The Wiskott-Aldrich syndrome protein (WASP) family of molecules integrates upstream signalling events with changes in the actin cytoskeleton. N-WASP has been implicated both in the formation of cell-surface projections (filopodia) required for cell movement and in the actin-based motility of intracellular pathogens. To examine N-WASP function we have used homologous recombination to inactivate the gene encoding murine N-WASP. Whereas N-WASP-deficient embryos survive beyond gastrulation and initiate organogenesis, they have marked developmental delay and die before embryonic day 12. N-WASP is not required for the actin-based movement of the intracellular pathogen Listeria but is absolutely required for the motility of Shigella and vaccinia virus. Despite these distinct defects in bacterial and viral motility, N-WASP-deficient fibroblasts spread by using lamellipodia and can protrude filopodia. These results imply a crucial and non-redundant role for N-WASP in murine embryogenesis and in the actin-based motility of certain pathogens but not in the general formation of actin-containing structures.

PMID:
11584271
DOI:
10.1038/ncb1001-897
[Indexed for MEDLINE]

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