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

Nature cell biology | Oct 3, 2001

http://www.ncbi.nlm.nih.gov/pubmed/11584271

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.

Pubmed ID: 11584271 RIS Download

Mesh terms: Actins | Animals | Cell Line | Cell Line, Transformed | Cell Movement | Cell Surface Extensions | Embryonic and Fetal Development | Fibroblasts | Gene Targeting | Listeria | Mice | Microscopy, Fluorescence | Nerve Tissue Proteins | Platelet-Derived Growth Factor | Recombination, Genetic | Shigella flexneri | Vaccinia virus | Wiskott-Aldrich Syndrome Protein, Neuronal

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Associated grants

  • Agency: NIAID NIH HHS, Id: R01 AI023262
  • Agency: NIAID NIH HHS, Id: R01 AI034276

Mouse Genome Informatics (Data, Gene Annotation)

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