N-WASP deficiency reveals distinct pathways for cell surface projections and microbial actin-based motility.
Document Type
Article
Publication Date
2001
First Page
897
Last Page
904
JAX Source
Nat Cell Biol 2001 Oct; 3(10):897-904.
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.
Recommended Citation
Snapper SB,
Takeshima F,
Anton I,
Liu CH,
Thomas SM,
Nguyen D,
Dudley D,
Fraser H,
Purich D,
Lopez IM,
Klein C,
Davidson L,
Bronson R,
Mulligan RC,
Southwick F,
Geha R,
Goldberg MB,
Rosen FS,
Hartwig JH,
Alt FW.
N-WASP deficiency reveals distinct pathways for cell surface projections and microbial actin-based motility. Nat Cell Biol 2001 Oct; 3(10):897-904.