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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Focal adhesion kinase controls actin assembly via a FERM-mediated interaction with the Arp2/3 complex.

Networks of actin filaments, controlled by the Arp2/3 complex, drive membrane protrusion during cell migration. How integrins signal to the Arp2/3 complex is not well understood. Here, we show that focal adhesion kinase (FAK) and the Arp2/3 complex associate and colocalize at transient structures formed early after adhesion. Nascent lamellipodia, which originate at these structures, do not form in FAK-deficient cells, or in cells in which FAK mutants cannot be autophosphorylated after integrin engagement. The FERM domain of FAK binds directly to Arp3 and can enhance Arp2/3-dependent actin polymerization. Critically, Arp2/3 is not bound when FAK is phosphorylated on Tyr 397. Interfering peptides and FERM-domain point mutants show that FAK binding to Arp2/3 controls protrusive lamellipodia formation and cell spreading. This establishes a new function for the FAK FERM domain in forming a phosphorylation-regulated complex with Arp2/3, linking integrin signalling directly with the actin polymerization machinery.[1]

References

  1. Focal adhesion kinase controls actin assembly via a FERM-mediated interaction with the Arp2/3 complex. Serrels, B., Serrels, A., Brunton, V.G., Holt, M., McLean, G.W., Gray, C.H., Jones, G.E., Frame, M.C. Nat. Cell Biol. (2007) [Pubmed]
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