N-WASP deficiency reveals distinct pathways for cell surface projections and microbial actin-based motility.
Nat Cell Biol
; 3(10): 897-904, 2001 Oct.
Article
en En
| MEDLINE
| ID: mdl-11584271
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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Banco de datos:
MEDLINE
Asunto principal:
Movimiento Celular
/
Actinas
/
Extensiones de la Superficie Celular
/
Desarrollo Embrionario y Fetal
/
Proteínas del Tejido Nervioso
Límite:
Animals
Idioma:
En
Año:
2001
Tipo del documento:
Article