Author: ["Scott B. Snapper","Fuminao Takeshima","Inés Antón","Ching-Hui Liu","Sheila M. Thomas","Deanna Nguyen","Darryll Dudley","Hunter Fraser","Daniel Purich","Marco Lopez-Ilasaca","Christoph Klein","Laurie Davidson","Roderick Bronson","Richard C. Mulligan","Fred Southwick","Raif Geha","Marcia B. Goldberg","Fred S. Rosen","John H. Hartwig","Frederick W. Alt"]
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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.Cite this article
Snapper, S., Takeshima, F., Antón, I. et al. N-WASP deficiency reveals distinct pathways for cell surface projections and microbial actin-based motility. Nat Cell Biol 3, 897–904 (2001). https://doi.org/10.1038/ncb1001-897 