The Plexin-B1/Rac interaction inhibits PAK activation and enhances Sema4D ligand binding

  1. Haris G. Vikis1,
  2. Weiquan Li1, and
  3. Kun-Liang Guan1,2,3
  1. 1Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA; 2Institute of Gerontology, University of Michigan, Ann Arbor, Michigan 48109, USA

Abstract

The small GTPase Rac has been implicated in growth cone guidance mediated by semaphorins and their receptors. Here we demonstrate that plexin-B1, a receptor for Semaphorin4D (Sema4D), and p21-activated kinase (PAK) can compete for the interaction with active Rac and plexin-B1 can inhibit Rac-induced PAK activation. We have also demonstrated that expression of active Rac enhances the ability of plexin-B1 to interact with Sema4D. Active Rac stimulates the localization of plexin-B1 to the cell surface. The enhancement in Sema4D binding depends on the ability of Rac to bind plexin-B1. These observations support a model where signaling between Rac and plexin-B1 is bidirectional; Rac modulates plexin-B1 activity and plexin-B1 modulates Rac function.

Keywords

Footnotes

  • ↵3 Corresponding author.

  • E-MAIL kunliang{at}umich.edu; FAX (734) 763-4581.

  • Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.966402.

    • Received November 30, 2001.
    • Accepted February 13, 2002.
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  1. doi: 10.1101/gad.966402 Genes & Dev. 16: 836-845 Cold Spring Harbor Laboratory Press

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