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

William E. Lowry, Jianyun Huang, Yong Chao Ma, Shariq Ali, Dongxia Wang, Daniel M. Williams, Masato Okada, Philip A. Cole, Xin Yun Huang

Research output: Contribution to journalArticlepeer-review

65 Scopus citations


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 (Gβγ, Gα12, Gα13, and Gαq)-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 Gβγ 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.

Original languageEnglish (US)
Pages (from-to)733-744
Number of pages12
JournalDevelopmental Cell
Issue number6
StatePublished - 2002
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Developmental Biology
  • Cell Biology


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