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Vol. 17, Issue 5, 2236-2242, May 2006

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Proteasome-mediated Degradation of Rac1-GTP during Epithelial Cell Scattering

Emma A. Lynch ^*, Jennifer Stall ^*, Gudila Schmidt , Philippe Chavrier , and Crislyn D'Souza-Schorey ^*

^* Department of Biological Sciences and the Walther Cancer Institute, University of Notre Dame, Notre Dame, IN 46556; Institut fur Experimentelle und Klinische Pharmakologie und Toxikologie der Albert-Ludwigs-Universitat Freiburg, D-79104 Freiburg, Germany; and Membrane and Cytoskeleton Dynamics Group, Institute Curie, 75248 Paris, France

Submitted August 18, 2005; Revised February 6, 2006; Accepted February 8, 2006
Monitoring Editor: Asma Nusrat

Epithelial cells disassemble their adherens junctions and "scatter" during processes such as tumor cell invasion as well as some stages of embryonic development. Control of actin polymerization is a powerful mechanism for regulating the strength of cell–cell adhesion. In this regard, studies have shown that sustained activation of Rac1, a well-known regulator of actin dynamics, results in the accumulation of polymerized actin at cell–cell contacts in epithelia and an increase in E-cadherin–mediated adhesion. Here we show that active Rac1 is ubiquitinated and subject to proteasome-mediated degradation during the early stages of epithelial cell scattering. These findings delineate a mechanism for the down-regulation of Rac1 in the disassembly of epithelial cell–cell contacts and support the emerging theme that UPS-mediated degradation of the Rho family GTPases may serve as an efficient mechanism for GTPase deactivation in the sustained presence of Dbl-exchange factors.

The online version of this article contains supplemental material at MBC Online (http://www.molbiolcell.org).

Address correspondence to: Crislyn D'Souza-Schorey (D'Souza-Schorey.1{at}nd.edu).

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