Evidence map›Paper›PMID 27530917›Full record

ArticleNature communications2016

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, Ho-Ryun Chung

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 99 citations in OpenAlex.

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  6. Histone bivalency in CNS development.Genes & development · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Sarah KinkleyOtto-Warburg-Laboratory: Epigenomics, Max Planck Institute for Molecular Genetics, Ihnestrasse 63-73, 14195 Berlin, Germany.
Johannes HelmuthOtto-Warburg-Laboratory: Epigenomics, Max Planck Institute for Molecular Genetics, Ihnestrasse 63-73, 14195 Berlin, Germany.ORCID http://orcid.org/0000-0002-5380-4577
Julia K PolanskyExperimental Rheumatology, German Rheumatism Research Center Berlin, Charitéplatz 1, 10117 Berlin, Germany.
Ilona DunkelOtto-Warburg-Laboratory: Epigenomics, Max Planck Institute for Molecular Genetics, Ihnestrasse 63-73, 14195 Berlin, Germany.
Gilles GasparoniThe Department of Genetics and Epigenetics, University of Saarland, Campus A2.4 66123 Saarbrücken, Germany.
Sebastian FröhlerThe Laboratory of Functional Genomics and Systems Biology, Max Delbruck Centrum for Molecular Medicine, Robert-Rössle-Strasse 10, 13125 Berlin, Germany.
Wei ChenThe Laboratory of Functional Genomics and Systems Biology, Max Delbruck Centrum for Molecular Medicine, Robert-Rössle-Strasse 10, 13125 Berlin, Germany.
Jörn WalterThe Department of Genetics and Epigenetics, University of Saarland, Campus A2.4 66123 Saarbrücken, Germany.
Alf HamannExperimental Rheumatology, German Rheumatism Research Center Berlin, Charitéplatz 1, 10117 Berlin, Germany.ORCID http://orcid.org/0000-0003-1518-5717
Ho-Ryun ChungOtto-Warburg-Laboratory: Epigenomics, Max Planck Institute for Molecular Genetics, Ihnestrasse 63-73, 14195 Berlin, Germany.ORCID http://orcid.org/0000-0002-4132-0911
Max Planck Institute for Molecular Genetics · DEGerman Rheumatism Research Centre · DEMax Delbrück Center · DESaarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Base SequenceCD4-Positive T-LymphocytesChromatin ImmunoprecipitationCpG IslandsDNA MethylationEpigenesis, GeneticGenome, HumanHistonesHumansLysineMethylationModels, GeneticPromoter Regions, GeneticSequence Analysis, DNATranscription Initiation SiteHistonesLysine

Identifiers

PMID27530917
PMCPMC4992058
OpenAlexW2511791445

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.