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Dev Cell. 2002 Jun;2(6):733-44.

Csk, a critical link of g protein signals to actin cytoskeletal reorganization.

Author information

1
Department of Physiology, Cornell University, Weill Medical College, New York, New York 10021, USA.

Abstract

Heterotrimeric G proteins can signal to reorganize the actin cytoskeleton, but the mechanism is unclear. Here we report that, in tyrosine kinase Csk-deficient mouse embryonic fibroblast cells, G protein (Gbetagamma, Galpha(12), Galpha(13), and Galpha(q))-induced, and G protein-coupled receptor-induced, actin stress fiber formation was completely blocked. Reintroduction of Csk into Csk-deficent cells restored the G protein-induced actin stress fiber formation. Chemical rescue experiments with catalytic mutants of Csk demonstrated that the catalytic activity of Csk was required for this process. Furthermore, we uncovered that Gbetagamma can both translocate Csk to the plasma membrane and directly increase Csk kinase activity. Our genetic and biochemical studies demonstrate that Csk plays a critical role in mediating G protein signals to actin cytoskeletal reorganization.

PMID:
12062086
DOI:
10.1016/s1534-5807(02)00175-2
[Indexed for MEDLINE]
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