期刊
SCIENCE
卷 293, 期 5532, 页码 1133-1136出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.293.5532.1133
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资金
- NIGMS NIH HHS [5-T32-GM07367, 1RO1GM54605] Funding Source: Medline
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 (p) under bar 300/(C) under bar BP-(a) under bar ssociated (f) under bar actors (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-P 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.
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