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Binding of YY1 to the Proximal Region of the Murine Beta 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

Received 10 March 2006/ Returned for modification 19 April 2006/ Accepted 28 August 2006

Virus-induced activation of the beta interferon (IFN-ß) 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 Yin Yang 1 (YY1) binds the murine IFN-ß promoter at two sites (–122 and –90) regulating 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-ß promoter region after virus infection. A 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-ß promoter through its –90 site via histone deacetylation. Here we demonstrate that, in vivo, the binding of YY1 to the –90 site is constant all through virus infection whereas the binding of YY1 to the –122 site is activated after infection. We discuss here the capacity of YY1 to either repress (through histone deacetylase recruitment) or activate (through CBP recruitment) IFN-ß gene expression according to the occupancy of either only its –90 site or both its –122 and –90 sites.

Published ahead of print on 5 September 2006.

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