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- Title
Coordination of a transcriptional switch by HMGI(Y) acetylation.
- Authors
Munshi, N; Agalioti, T; Lomvardas, S; Merika, M; Chen, G; Thanos, D
- Abstract
Dynamic control of interferon-beta (IFN-beta) 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-beta 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.
- Publication
Science (New York, N.Y.), 2001, Vol 293, Issue 5532, p1133
- ISSN
0036-8075
- Publication type
Journal Article
- DOI
10.1126/science.293.5532.1133