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Mol. Cell. Biol. doi:10.1128/MCB.00420-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Binding of YY1 to the proximal region of the murine interferon promoter is essential to allow CBP-recruitment and K8H4/K14H3 acetylation on the promoter region after virus infection

Régulation de la Transcription et Maladies Génétiques. CNRS UPR2228. UFR Biomédicale. 45 rue des Saints-Pères, 75270 Paris cedex 06, France

^* To whom correspondence should be addressed. Email: bonnefoy{at}biomedicale.univ-paris5.fr.

	Abstract

Virus-induced activation of the interferon- (IFN-) gene requires orderly recruitment of chromatin remodeling complexes and time-regulated acetylation of histone residues K8H4 and K14H3 on the promoter region. We have previously shown that transcription factor YY1 binds the murine IFN- promoter at two sites (-122 and -90) regulating the promoter transcriptional capacity with a dual activator/repressor role. In this work we demonstrate that both YY1 -122 and -90 sites are required for CBP-recruitment and K8H4/K14H3 acetylation to take place on the IFN- promoter region after virus infection. Single point mutation introduced at either one of these two sites inhibiting YY1 binding, completely disrupted CBP recruitment and K8H4/K14H3 acetylation independently of HMGI or IRF3 binding to the promoter. We have previously demonstrated that YY1 represses the transcriptional capacity of the IFN- promoter through its -90 site via histone deacetylation. Here we demonstrate that in vivo, binding of YY1 to the -90 site is constant all through virus infection whereas binding of YY1 to the -122 site is activated after infection. We discuss here the capacity of YY1 to either repress (through HDAC recruitment) or activate (through CBP recruitment) IFN- gene expression according to the occupancy of either only its -90 site or both its -122 and the -90 sites.

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