Contingent phosphorylation/dephosphorylation provides a mechanism of molecular memory in WASP

Eduardo Torres, Michael K. Rosen

Research output: Contribution to journalArticle

132 Scopus citations

Abstract

Cells can retain information about previous stimuli to produce distinct future responses. The biochemical mechanisms by which this is achieved are not well understood. The Wiskott-Aldrich syndrome protein (WASP) is an effector of the Rho-family GTPase Cdc42, whose activation leads to stimulation of the actin nucleating assembly, Arp2/3 complex. We demonstrate that efficient phosphorylation and dephosphorylation of WASP at Y291 are both contingent on binding to activated Cdc42. Y291 phosphorylation increases the basal activity of WASP toward Arp2/3 complex and enables WASP activation by new stimuli, SH2 domains of Src-family kinases. The requirement for contingency in both phosphorylation and dephosphorylation enables long-term storage of information by WASP following decay of GTPase signals. This biochemical circuitry allows WASP to respond to the levels and timing of GTPase and kinase signals. It provides mechanisms to specifically achieve transient or persistent actin remodeling, as well as long-lasting potentiation of actin-based responses to kinases.

Original languageEnglish (US)
Pages (from-to)1215-1227
Number of pages13
JournalMolecular cell
Volume11
Issue number5
DOIs
StatePublished - May 1 2003

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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