reChIP-seq reveals widespread bivalency of H3K4me3 and H3K27me3 in CD4+ memory T cells

Sarah Kinkley, Johannes Helmuth, Julia K. Polansky, Ilona Dunkel, Gilles Gasparoni, Sebastian Fröhler, Wei Chen, Jörn Walter, Alf Hamann and Ho-Ryun Chung ()
Additional contact information
Sarah Kinkley: Otto-Warburg-Laboratory: Epigenomics, Max Planck Institute for Molecular Genetics, Ihnestrasse 63-73
Johannes Helmuth: Otto-Warburg-Laboratory: Epigenomics, Max Planck Institute for Molecular Genetics, Ihnestrasse 63-73
Julia K. Polansky: Experimental Rheumatology, German Rheumatism Research Center Berlin, Charitéplatz 1
Ilona Dunkel: Otto-Warburg-Laboratory: Epigenomics, Max Planck Institute for Molecular Genetics, Ihnestrasse 63-73
Gilles Gasparoni: University of Saarland, Campus A2.4
Sebastian Fröhler: The Laboratory of Functional Genomics and Systems Biology, Max Delbruck Centrum for Molecular Medicine
Wei Chen: The Laboratory of Functional Genomics and Systems Biology, Max Delbruck Centrum for Molecular Medicine
Jörn Walter: University of Saarland, Campus A2.4
Alf Hamann: Experimental Rheumatology, German Rheumatism Research Center Berlin, Charitéplatz 1
Ho-Ryun Chung: Otto-Warburg-Laboratory: Epigenomics, Max Planck Institute for Molecular Genetics, Ihnestrasse 63-73

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract The combinatorial action of co-localizing chromatin modifications and regulators determines chromatin structure and function. However, identifying co-localizing chromatin features in a high-throughput manner remains a technical challenge. Here we describe a novel reChIP-seq approach and tailored bioinformatic analysis tool, normR that allows for the sequential enrichment and detection of co-localizing DNA-associated proteins in an unbiased and genome-wide manner. We illustrate the utility of the reChIP-seq method and normR by identifying H3K4me3 or H3K27me3 bivalently modified nucleosomes in primary human CD4+ memory T cells. We unravel widespread bivalency at hypomethylated CpG-islands coinciding with inactive promoters of developmental regulators. reChIP-seq additionally uncovered heterogeneous bivalency in the population, which was undetectable by intersecting H3K4me3 and H3K27me3 ChIP-seq tracks. Finally, we provide evidence that bivalency is established and stabilized by an interplay between the genome and epigenome. Our reChIP-seq approach augments conventional ChIP-seq and is broadly applicable to unravel combinatorial modes of action.

Date: 2016
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms12514 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12514

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms12514

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().