Coordination of a transcriptional switch by HMGI(Y) acetylation

N. Munshi, T. Agalioti, S. Lomvardas, M. Merika, G. Chen, D. Thanos

Research output: Contribution to journalArticlepeer-review

185 Scopus citations


Dynamic control of interferon-β (IFN-β) gene expression requires the regulated assembly and disassembly of the enhanceosome, a higher-order nucleoprotein complex formed in response to virus infection. The enhanceosome activates transcription by recruiting the histone acetyltransferase proteins CREB binding protein (CBP) and p300/CBP-associated factors (PCAF)/GCN5, which, in addition to modifying histones, acetylate HMGI(Y), the architectural component required for enhanceosome assembly. We show that the accurate execution of the IFN-β transcriptional switch depends on the ordered acetylation of the high-mobility group I protein HMGI(Y) by PCAF/GCN5 and CBP, which acetylate HMGI(Y) at distinct lysine residues on endogenous promoters. Whereas acetylation of HMGI(Y) by CBP at lysine-65 destabilizes the enhanceosome, acetylation of HMGI(Y) by PCAF/GCN5 at lysine-71 potentiates transcription by stabilizing the enhanceosome and preventing acetylation by CBP.

Original languageEnglish (US)
Pages (from-to)1133-1136
Number of pages4
Issue number5532
StatePublished - Aug 10 2001

ASJC Scopus subject areas

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