Genome-wide Mapping of HATs and HDACs Reveals Distinct Functions in Active and Inactive Genes

被引：1216

作者：

Wang, Zhibin ^{[1
]}

Zang, Chongzhi ^{[2
]}

Cui, Kairong ^{[1
]}

Schones, Dustin E. ^{[1
]}

Barski, Artem ^{[1
]}

Peng, Weiqun ^{[2
]}

Zhao, Keji ^{[1
]}

机构：

[1] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA

[2] George Washington Univ, Dept Phys, Washington, DC 20052 USA

来源：

CELL | 2009年 / 138卷 / 05期

基金：

美国国家卫生研究院;

关键词：

HISTONE DEACETYLASE; CHROMATIN SIGNATURES; CODING REGIONS; COMPLEX; YEAST; ACETYLATION; METHYLATION; ACETYLTRANSFERASE; TRANSCRIPTION; NUCLEOSOMES;

D O I：

10.1016/j.cell.2009.06.049

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Histone acetyltransferases (HATs) and deacetylases (HDACs) function antagonistically to control histone acetylation. As acetylation is a histone mark for active transcription, HATs have been associated with active and HDACs with inactive genes. We describe here genome-wide mapping of HATs and HDACs binding on chromatin and find that both are found at active genes with acetylated histones. Our data provide evidence that HATs and HDACs are both targeted to transcribed regions of active genes by phosphorylated RNA Pol II. Furthermore, the majority of HDACs in the human genome function to reset chromatin by removing acetylation at active genes. Inactive genes that are primed by MLL-mediated histone H3K4 methylation are subject to a dynamic cycle of acetylation and deacetylation by transient HAT/HDAC binding, preventing Pol II from binding to these genes but poising them for future activation. Silent genes without any H3K4 methylation signal show no evidence of being bound by HDACs.

引用

页码：1019 / 1031

页数：13

共 54 条

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