H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction
- Gillian C.A. Taylor,
- Ragnhild Eskeland1,
- Betül Hekimoglu-Balkan,
- Madapura M. Pradeepa2 and
- Wendy A. Bickmore2
- MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine at University of Edinburgh, Edinburgh EH4 2XU, United Kingdom
Abstract
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.
Footnotes
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↵2 Corresponding authors
E-mail Wendy.Bickmore{at}igmm.ed.ac.uk
E-mail Pradeepa.MM{at}igmm.ed.ac.uk
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[Supplemental material is available for this article.]
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Article published online before print. Article, supplemental material, and publication date are at http://www.genome.org/cgi/doi/10.1101/gr.155028.113.
- Received January 16, 2013.
- Accepted August 28, 2013.
This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genome.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 3.0 Unported), as described at http://creativecommons.org/licenses/by-nc/3.0/.
