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Snapper, S.B. et al.

Snapper, Takeshima, Antón, Liu, Thomas, Nguyen, Dudley, Fraser, Purich, Lopez-Ilasaca, Klein, Davidson, Bronson, Mulligan, Southwick, Geha, Goldberg, Rosen, Hartwig, Alt,

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

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.[1]

References

N-WASP deficiency reveals distinct pathways for cell surface projections and microbial actin-based motility. Snapper, S.B., Takeshima, F., Antón, I., Liu, C.H., Thomas, S.M., Nguyen, D., Dudley, D., Fraser, H., Purich, D., Lopez-Ilasaca, M., Klein, C., Davidson, L., Bronson, R., Mulligan, R.C., Southwick, F., Geha, R., Goldberg, M.B., Rosen, F.S., Hartwig, J.H., Alt, F.W. Nat. Cell Biol. (2001) [Pubmed]

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