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Journal of Virology, March 2003, p. 2903-2914, Vol. 77, No. 5
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.5.2903-2914.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Transcription Factor YY1 Binds to the Murine Beta Interferon Promoter and Regulates Its Transcriptional Capacity with a Dual Activator/Repressor Role

Laure Weill, Elena Shestakova, and Eliette Bonnefoy*

Régulation de la Transcription et Maladies Génétiques, CNRS UPR2228, UFR Biomédicale, 75270 Paris cedex 06, France

Received 6 August 2002/ Accepted 20 November 2002

The induction of the beta interferon (IFN-ß) gene constitutes one of the first responses of the cell to virus infection. Its regulation is achieved through an intricate combination of virus-induced binding of transcription factors and local chromatin remodeling. In this work, we demonstrate that transcription factor YY1, known to interact with histone deacetylases (HDAC) and histone acetyltransferases, has a dual activator/repressor role during the regulation of the IFN-ß promoter activity. We show that YY1 specifically binds in vitro and in vivo to the murine IFN-ß promoter at positions -90 and -122. Overexpression of YY1 strongly repressed the transcriptional capacity of a stably integrated IFN-ß promoter fused to a chloramphenicol acetyltransferase reporter gene as well as the endogenous IFN activity of murine L929 cells via an HDAC activity. Stably integrated IFN-ß promoters mutated at the -90 site were no longer repressed by YY1, could no longer be activated by trichostatin A, displayed a retarded postinduction turn off, and a reduced virus-induced activity. Introduction of a mutation at the -122 site did not affect YY1-induced repression, but promoters with this mutation displayed a reduced virus-induced activity. Stably integrated full-length promoters (from position -330 to +20) mutated at both YY1-binding sites displayed extremely reduced promoter activities. We conclude that YY1 has a dual activator/repressor role on IFN-ß promoter activity depending on its binding site and time after infection.

* Corresponding author. Mailing address: Régulation de la Transcription et Maladies Génétiques, CNRS UPR2228, UFR Biomédicale, 45 rue des Saints-Pères, 75270 Paris cedex 06, France. Phone: (33) 1-42-86-22-76. Fax: (33) 1-42-86-20-42. E-mail: bonnefoy{at}biomedicale.univ-paris5.fr.

Journal of Virology, March 2003, p. 2903-2914, Vol. 77, No. 5
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.5.2903-2914.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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