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J. Biol. Chem., Vol. 280, Issue 1, 401-407, January 7, 2005

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The Repressor Element Silencing Transcription Factor (REST)-mediated Transcriptional Repression Requires the Inhibition of Sp1^*

Valérie Plaisance, Guy Niederhauser, Fayçal Azzouz, Vincent Lenain, Jacques-Antoine Haefliger, Gérard Waeber, and Amar Abderrahmani, Supported by an ALFEDIAM grant and the Swiss National Science Foundation Grant 3100A0-105425¶

From the Department of Internal Medicine and Department of Cellular Biology and Morphology, University of Lausanne, 1005 Lausanne, Switzerland

The terminal differentiation of neuronal and pancreatic -cells requires the specific expression of genes that are targets of an important transcriptional repressor named RE-1 silencing transcription factor (REST). The molecular mechanism by which these REST target genes are expressed only in neuronal and -cells and are repressed by REST in other tissues is a central issue in differentiation program of neuronal and -cells. Herein, we showed that the transcriptional factor Sp1 was required for expression of most REST target genes both in insulin-secreting cells and neuronal-like cells where REST is absent. Inhibition of REST in a non- and a non-neuronal cell model restored the transcriptional activity of Sp1. This activity was also restored by trichostatin A indicating the requirement of histone deacetylases for the REST-mediated silencing of Sp1. Conversely, exogenous introduction of REST blocked Sp1-mediated transcriptional activity. The REST inhibitory effect was mediated through its C-terminal repressor domain, which could interact with Sp1. Taken together, these data show that the inhibition of Sp1 by REST is required for the silencing of its target genes expression in non-neuronal and in non--cells. We conclude that the interplay between REST and Sp1 determines the cell-specific expression of REST target genes.

Received for publication, October 18, 2004

^* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

These authors contributed equally to this work.

Supported by the Swiss National Science Foundation Grants 32-066892.01, the Juvenile Diabetes Research Foundation Grant 1-2001-555, and the Placide Nicod and Octav Botnar Foundations.

^¶ To whom correspondence should be addressed: Institute of Cellular Biology and Morphology, University of Lausanne, 1005 Lausanne, Switzerland. Tel.: 41-21-692-52-91; Fax: 41-21-314-51-05; E-mail: Amar.Abderrahmani{at}ibcm.unil.ch.

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