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Originally published In Press as doi:10.1074/jbc.M111627200 on February 21, 2002

J. Biol. Chem., Vol. 277, Issue 18, 15376-15384, May 3, 2002
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Vav1 Couples T Cell Receptor to Serum Response Factor-dependent Transcription via a MEK-dependent Pathway*

Céline CharvetDagger §, Patrick Auberger, Sophie Tartare-Deckert||, Alain BernardDagger , and Marcel DeckertDagger **

From Dagger  INSERM U343, IFR50, Hôpital de l'Archet, 06202 Nice Cedex 3 and  INSERM U526 and || INSERM U385, IFR50, Faculté de Médecine, Avenue de Valombrose, 06107 Nice Cedex 2, France

The Vav family of guanine nucleotide exchange factors for Rho family GTPases plays a critical role in lymphocyte proliferation, gene transcription, and cytoskeleton reorganization following immunoreceptor stimulation. However, its role in immediate early gene activation is unclear. In this study, we have investigated the mechanisms by which Vav1 can regulate c-fos serum response element transcriptional activity. We show that T cell antigen receptor (TCR) stimulation induces the phosphorylation of serum response factor (SRF) on serine 103 and increases the binding of SRF complexes on serum response element in a MEK- and p38-dependent pathway. The physiological relevance of our findings is supported by the inhibition of the interleukin-2 gene transcriptional activity by a dominant negative SRF mutant. Overexpression of Vav1, which partially mimics TCR stimulation, promotes SRF-dependent transcription, and dominant negative Vav1 mutants block SRF activation by TCR. SRF activation by Vav1 occurs through a signaling cascade consisting of Rac1/Cdc42 and the serine/threonine kinases Pak1 and MEK, but independently of the phosphatidylinositol 3-kinase pathway. Interestingly, Vav2 also enhances SRF through Rho GTPases, suggesting that Vav proteins are general regulators of SRF activation in lymphocytes. This report establishes Vav proteins as a direct link between antigen receptors and SRF-dependent early gene expression.

* This work was supported in part by INSERM, the Fondation pour la Recherche Médicale, and the Association pour la Recherche sur le Cancer.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Recipient of a doctoral fellowship from the Ministère de l'Enseignement Supérieur et de la Recherche.

** To whom correspondence should be addressed: INSERM U343, IFR50, Hôpital de l'Archet, 06202 Nice Cedex 3, France. Tel.: 33-4-92-15-77-00; Fax: 33-4-92-15-77-09; E-mail: deckert@unice.fr.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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