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First published online September 17, 2008

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WASP function goes live

Wiskott-Aldrich syndrome is a primary immunodeficiency that results from defective expression of the haematopoietically restricted Wiskott-Aldrich syndrome protein (WASP). WASP-defective cells have a perturbed migratory capacity in vitro – WASPs might also have an integral role in leukocyte motility in vivo, but it has not been possible to live-image the relevant cell migrations. Now, Paul Martin and colleagues (p. 3196) take advantage of the translucency of zebrafish embryos and larvae to develop a model to investigate the in vivo function of Wasp1 in migrating leukocytes in a wound inflammatory response. Using morpholino knockdown of Wasp1, the authors show that the mechanism used by neutrophils and macrophages to orient towards wound signals is impaired, thereby dramatically disrupting the wound inflammatory response. Wasp1 deficiency leads to a reduction in the velocity of migration of these cells, and the leukocytes often fail in their ability to choose the correct leading-edge pseudopodia, leading to defective chemotaxis. Similar results were obtained with a knockout of Wasp1 using a TILLING (targeting-induced local lesions in genomes) approach. These results provide insight into how WASPs regulate leukocyte migration in vivo.

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Related articles in JCS:

Analysis of WASp function during the wound inflammatory response – live-imaging studies in zebrafish larvae

Ana Cvejic, Chris Hall, Magdalena Bak-Maier, Maria Vega Flores, Phil Crosier, Michael J. Redd, and Paul Martin
JCS 2008 121: 3196-3206. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?