Format

Send to

Choose Destination
Mol Cell. 1999 Jan;3(1):125-9.

Virus infection leads to localized hyperacetylation of histones H3 and H4 at the IFN-beta promoter.

Author information

1
Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA.

Abstract

Transcriptional activation of the human interferon-beta (IFN-beta) gene by virus infection requires the assembly of a higher order nucleoprotein complex, the enhanceosome, which consists of the transcriptional activators NF-kappa B (p50/p65), ATF-2/c-jun, IRF-3 and IRF-7, architectural protein HMGI(Y), and the coactivators p300 and CBP. In this report, we show that virus infection of cells results in a dramatic hyperacetylation of histones H3 and H4 that is localized to the IFN-beta promoter. Furthermore, expressing a truncated version of IRF-3, which lacks a p300/CBP interaction domain, suppresses both histone hyperacetylation and activation of the IFN-beta gene. Thus, coactivator-mediated localized hyperacetylation of histones may play a crucial role in inducible gene expression.

PMID:
10024886
DOI:
10.1016/s1097-2765(00)80181-1
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center