H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction

被引:136
作者
Taylor, Gillian C. A. [1 ]
Eskeland, Ragnhild [1 ]
Hekimoglu-Balkan, Betuel [1 ]
Pradeepa, Madapura M. [1 ]
Bickmore, Wendy A. [1 ]
机构
[1] Univ Edinburgh, MRC Human Genet Unit, MRC Inst Genet & Mol Med, Edinburgh EH4 2XU, Midlothian, Scotland
基金
英国医学研究理事会;
关键词
DROSOPHILA MSL COMPLEX; H4 TAIL ACETYLATIONS; MALE X-CHROMOSOME; HISTONE H4; DOSAGE COMPENSATION; NUCLEAR REORGANIZATION; H4-K16; ACETYLATION; KEY REGULATOR; MOF; DISTINCT;
D O I
10.1101/gr.155028.113
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Compared with histone H3, acetylation of H4 tails has not been well studied, especially in mammalian cells. Yet, H4K16 acetylation is of particular interest because of its ability to decompact nucleosomes in vitro and its involvement in dosage compensation in flies. Here we show that, surprisingly, loss of H4K16 acetylation does not alter higher-order chromatin compaction in vivo in mouse embryonic stem cells (ESCs). As well as peaks of acetylated H4K16 and KAT8 histone acetyltransferase at the transcription start sites of expressed genes, we report that acetylation of H4K16 is a new marker of active enhancers in ESCs and that some enhancers are marked by H3K4me1, KAT8, and H4K16ac, but not by acetylated H3K27 or EP300, suggesting that they are novel EP300 independent regulatory elements. Our data suggest a broad role for different histone acetylation marks and for different histone acetyltransferases in long-range gene regulation.
引用
收藏
页码:2053 / 2065
页数:13
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