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Originally published In Press as doi:10.1074/jbc.M100481200 on January 22, 2001

J. Biol. Chem., Vol. 276, Issue 16, 12781-12784, April 20, 2001
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Chromatin Is Permissive to TATA-binding Protein (TBP)-mediated Transcription Initiation*

Eumorphia RemboutsikaDagger , Xavier Jacq§, and Làszlò Tora

From the Department of Transcriptional and Post-transcriptional Control of Gene Regulation, Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, BP 163, F-67404 Illkirch Cedex, Communauté Urbaine de Strasbourg, France

Preinitiation complex assembly is nucleated by the binding of TFIID to the promoters of protein coding genes transcribed by RNA polymerase II. TFIID is comprised of the TATA-binding protein (TBP) and TBP-associated factors (TAFIIs). We investigated the transcription properties of TBP and TFIID on chromatin templates. On naked templates both TBP and purified TFIID are able to initiate basal transcription. However, on chromatin templates only TBP mediates transcription initiation in a heat-treated extract, whereas TFIID does not. Moreover, TBP-mediated chromatin transcription is blocked in a nontreated extract. These observations suggest that a chromatin-targeted repressor is present in crude extracts and that chromatin per se is not refractory to transcription mediated by TBP. As TBP can function through TAFII-independent and TAFII-dependent pathways, the repression of TBP-mediated basal transcription may be an additional level to the control of Pol II transcription initiation on chromatin.

* This work was supported by funds from INSERM, CNRS, Hôpital Universitaire de Strasbourg, Association pour la Recherche sur le Cancer, Fondation pour la Recherche Médicale, Ligue Nationale contre le Cancer, and Human Frontier Science Program (Grant RG 196/98).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.

Dagger Supported by a Human Capital and Mobility fellowship from the European Community and by a grant from the Fondation pour la Recherche Medicale. Present address: Div. of Developmental Genetics, National Inst. for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA United Kingdom.

§ Present address: Target Identification, Dept. of Internal Medicine, Sanofi-Synthelabo, 92500  Rueil-Malmaison, France.

To whom correspondence should be addressed. Tel.: 33-3-88-65-34-44; Fax: 33-3-88-65-32-01; E-mail: laszlo@igbmc.u-strasbg.fr.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.


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