N-WASP deficiency reveals distinct pathways for cell surface projections and microbial actin-based motility - PubMed (original) (raw)

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

doi: 10.1038/ncb1001-897.

F Takeshima, I Antón, C H Liu, S M Thomas, D Nguyen, D Dudley, H Fraser, D Purich, M Lopez-Ilasaca, C Klein, L Davidson, R Bronson, R C Mulligan, F Southwick, R Geha, M B Goldberg, F S Rosen, J H Hartwig, F W Alt

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

S B Snapper et al. Nat Cell Biol. 2001 Oct.

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.

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