Mechanism of regulation of WAVE1-induced actin nucleation by Rac1 and Nck

Sharon Eden, Rajat Rohatgi, Alexandre V. Podtelejnikov, Matthias Mann and Marc W. Kirschner ()
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Sharon Eden: Harvard Medical School
Rajat Rohatgi: Harvard Medical School
Alexandre V. Podtelejnikov: University of Southern Denmark-Odense Campusvej 55
Matthias Mann: University of Southern Denmark-Odense Campusvej 55
Marc W. Kirschner: Harvard Medical School

Nature, 2002, vol. 418, issue 6899, 790-793

Abstract: Abstract Rac signalling to actin—a pathway that is thought to be mediated by the protein Scar/WAVE (WASP (Wiskott–Aldrich syndrome protein)-family verprolin homologous protein)—has a principal role in cell motility. In an analogous pathway, direct interaction of Cdc42 with the related protein N-WASP stimulates actin polymerization1. For the Rac–WAVE pathway, no such direct interaction has been identified. Here we report a mechanism by which Rac and the adapter protein Nck activate actin nucleation through WAVE1. WAVE1 exists in a heterotetrameric complex that includes orthologues of human PIR121 (p53-inducible messenger RNA with a relative molecular mass (Mr) of 140,000), Nap125 (NCK-associated protein with an Mr of 125,000) and HSPC300. Whereas recombinant WAVE1 is constitutively active, the WAVE1 complex is inactive. We therefore propose that Rac1 and Nck cause dissociation of the WAVE1 complex, which releases active WAVE1–HSPC300 and leads to actin nucleation.

Date: 2002
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DOI: 10.1038/nature00859

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