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Molecular and Cellular Biology, March 2003, p. 2151-2161, Vol. 23, No. 6
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.6.2151-2161.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

The TRE17 Oncogene Encodes a Component of a Novel Effector Pathway for Rho GTPases Cdc42 and Rac1 and Stimulates Actin Remodeling

Jeffrey M. Masuda-Robens,1 Sara N. Kutney,1 Hongwei Qi,2,{dagger} and Margaret M. Chou2*

Department of Pharmacology,and Department of Cell and Developmental Biology,1 University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-61602

Received 23 May 2002/ Returned for modification 5 July 2002/ Accepted 18 November 2002

The Rho family GTPases Cdc42 and Rac1 play fundamental roles in transformation and actin remodeling. Here, we demonstrate that the TRE17 oncogene encodes a component of a novel effector pathway for these GTPases. TRE17 coprecipitated specifically with the active forms of Cdc42 and Rac1 in vivo. Furthermore, the subcellular localization of TRE17 was dramatically regulated by these GTPases and mitogens. Under serum-starved conditions, TRE17 localized predominantly to filamentous structures within the cell. Epidermal growth factor (EGF) induced relocalization of TRE17 to the plasma membrane in a Cdc42-/Rac1-dependent manner. Coexpression of activated alleles of Cdc42 or Rac1 also caused complete redistribution of TRE17 to the plasma membrane, where it partially colocalized with the GTPases in filopodia and ruffles, respectively. Membrane recruitment of TRE17 by EGF or the GTPases was dependent on actin polymerization. Finally, we found that a C-terminal truncation mutant of TRE17 induced the accumulation of cortical actin, mimicking the effects of activated Cdc42. Together, these results identify TRE17 as part of a novel effector complex for Cdc42 and Rac1, potentially contributing to their effects on actin remodeling. The present study provides insights into the regulation and cellular function of this previously uncharacterized oncogene.

* Corresponding author. Mailing address: Department of Cell and Developmental Biology, 421 Curie Blvd., BRBII Rm. 1011, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6160. Phone: (215) 573-4126. Fax: (215) 898-9871. E-mail: mmc{at}mail.med.upenn.edu.

{dagger} Present address: GlaxoSmithKline, King of Prussia, PA 19406.

Molecular and Cellular Biology, March 2003, p. 2151-2161, Vol. 23, No. 6
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.6.2151-2161.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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