Evidence map›Paper›PMID 41778583›Full record

ArticleeLife2026

Acetylation of H3K115 is associated with fragile nucleosomes at CpG island promoters and active regulatory sites.

Yatendra Kumar, Dipta Sengupta, Elias T Friman, Robert S Illingworth, Manon Soleil, Zheng Fan, Hua Wang, Kristian Helin, Matthieu Gérard, Wendy A Bickmore

Abstract read
In one paragraph

Article in eLife, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Yatendra Kumar *MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, United Kingdom.ORCID https://orcid.org/0000-0001-8371-2887
Dipta Sengupta *MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, United Kingdom.ORCID https://orcid.org/0000-0002-7836-4774
Elias T FrimanMRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, United Kingdom.ORCID https://orcid.org/0000-0001-9944-6560
Robert S IllingworthMRC Centre for Regenerative Medicine, Institute for Regeneration and Repair, University of Edinburgh, Edinburgh, United Kingdom.
Manon SoleilUniversité Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC), Gif-sur-Yvette, France.ORCID https://orcid.org/0009-0000-4195-8993
Zheng FanDivision of Cancer Biology, The Institute of Cancer Research, London, United Kingdom.ORCID https://orcid.org/0000-0003-1934-2521
Hua WangDepartment of Lymphoma, Peking University Cancer Hospital and Institute, Peking University International Cancer Institute, Peking University Health Science Center, Beijing, China.ORCID https://orcid.org/0000-0002-1424-0270
Kristian HelinDivision of Cancer Biology, The Institute of Cancer Research, London, United Kingdom.
Matthieu GérardUniversité Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC), Gif-sur-Yvette, France.ORCID https://orcid.org/0000-0001-8956-0597
Wendy A BickmoreMRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, United Kingdom.ORCID https://orcid.org/0000-0001-6660-7735

Funding

Medical Research Council MC_UU_00035/7Swiss National Science Foundation P500PB_206805
6 · The paper itself

Abstract

Acetylation of lysine residues in the tail domain of histone H3 is well characterised, but lysine residues in the histone globular domain are also acetylated. Histone modifications in the globular domain have regulatory potential because of their impact on nucleosome stability but remain poorly characterised. In this study, we report the genome-wide distribution of acetylated H3 lysine 115 (H3K115ac), a residue on the lateral surface at the nucleosome dyad, using chromatin immunoprecipitation. In mouse embryonic stem cells, we find that detectable H3K115ac is enriched at the transcription start site of active CpG island promoters, but also at polycomb-repressed promoters prior to their subsequent activation during differentiation. By contrast, at enhancers, H3K115ac enrichment is dynamic, changing in line with gene activation and chromatin accessibility during differentiation. Most strikingly, we show that H3K115ac is detected as enriched on 'fragile' nucleosomes within nucleosome-depleted regions at promoters and active enhancers, where it coincides with transcription factor binding, and at CTCF-bound sites. These unique features suggest that H3K115ac correlates with, and could contribute to, nucleosome destabilisation and that it might be a valuable marker for identifying functionally important regulatory elements in mammalian genomes.

Indexed as

CpG IslandsHistonesNucleosomesPromoter Regions, GeneticAcetylationAnimalsCell DifferentiationChromatin ImmunoprecipitationLysineMiceMouse Embryonic Stem CellsHistonesLysineNucleosomeschromosomesCpG islandsCTCFenhancersgene expressionmousepolycombtranscription start site

Identifiers

PMID41778583
PMCPMC12959880

What OpenQuestion holds

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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.