JBC Transcription and Nuclear Factor Monoclonals

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Originally published In Press as doi:10.1074/jbc.C000568200 on September 5, 2000

J. Biol. Chem., Vol. 275, Issue 43, 33205-33208, October 27, 2000
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ACCELERATED PUBLICATION
Synergism between Transcription Factors TFE3 and Smad3 in Transforming Growth Factor-beta -induced Transcription of the Smad7 Gene*

Xianxin HuaDagger §, Zachary A. MillerDagger , Hassina Benchabane||, Jeffrey L. Wrana**, and Harvey F. LodishDagger Dagger Dagger

From the Dagger  Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142 and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139 and  Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada

Activation of transforming growth factor-beta (TGF-beta ) receptors triggers phosphorylation of Smad2 and Smad3. After binding to Smad4, the complex enters the nucleus and interacts with other transcription factors to activate gene transcription. Unlike other Smads, Smad7 inhibits phosphorylation of Smad2 and Smad3, and its transcription is induced by TGF-beta , suggesting a negative feedback loop. Here, we show that TFE3 and Smad3 synergistically mediate TGF-beta -induced transcription from the Smad7 promoter by binding to an E-box and two adjacent Smad binding elements (SBEs), respectively. A precise 3-base pair spacer between one SBE and the E-box is essential. Previously, we showed that a similar arrangement between a SBE and an E-box of an element is essential for TGF-beta -dependent transcription of the plasminogen activator inhibitor-1 gene (PAI-1) and that TGF-beta -induced phosphorylation of Smad3 triggers its association with TFE3. Thus, TFE3-Smad3 response elements may represent a common target for TGF-beta -induced gene expression.

* This work was supported by National Institutes of Health Grant CA63260 (to H. F. L.) and by Burroughs-Wellcome Career Award 1676 and Howard Temin Award CA78592-02 (to X. H.).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.

§ Current address: Abramson Family Cancer Research Inst., Dept. of Cancer Biology, University of Pennsylvania, Philadelphia, PA 19104.

|| Recipient of National Science and Engineering Council and "Fonds pour la formation de chercheurs et l'aide à la recherche" studentship.

** A Canadian Institute of Health Research investigator.

Dagger Dagger To whom correspondence should be addressed: The Whitehead Institute, Nine Cambridge Center, Cambridge, MA 02142. Tel.: 617-258-5216; Fax: 617-258-6768; E-mail: lodish@wi.mit.edu.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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