Regulation of transcription through acetylation of H3K122 on the lateral surface of the histone octamer.

Document Type

Article

Publication Date

2-14-2013

Keywords

Acetylation, Animals, Cell Line, Tumor, Eukaryota, Fibroblasts, Gene Expression Regulation, Histone Code, Histones, Humans, Mice, Models, Molecular, Nucleosomes, Receptors, Estrogen, Schizosaccharomyces, Transcription Initiation Site, Transcriptional Activation, p300-CBP Transcription Factors

JAX Source

Cell 2013 Feb; 152(4):859-72.

Volume

152

Issue

4

First Page

859

Last Page

872

ISSN

1097-4172

PMID

23415232

Abstract

Histone modifications are key regulators of chromatin function. However, little is known to what extent histone modifications can directly impact on chromatin. Here, we address how a modification within the globular domain of histones regulates chromatin function. We demonstrate that H3K122ac can be sufficient to stimulate transcription and that mutation of H3K122 impairs transcriptional activation, which we attribute to a direct effect of H3K122ac on histone-DNA binding. In line with this, we find that H3K122ac defines genome-wide genetic elements and chromatin features associated with active transcription. Furthermore, H3K122ac is catalyzed by the coactivators p300/CBP and can be induced by nuclear hormone receptor signaling. Collectively, this suggests that transcriptional regulators elicit their effects not only via signaling to histone tails but also via direct structural perturbation of nucleosomes by directing acetylation to their lateral surface. Cell 2013 Feb; 152(4):859-72.

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