Evidence map›Paper›PMID 26564795›Full record

ArticleMolecular biology of the cell2016

Epigenetic engineering shows that a human centromere resists silencing mediated by H3K27me3/K9me3.

Nuno M C Martins, Jan H Bergmann, Nobuaki Shono, Hiroshi Kimura, Vladimir Larionov, Hiroshi Masumoto, William C Earnshaw

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 40 citations in OpenAlex.

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  5. The dynamic centromere.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 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

7 authors at 4 institutions in 3 countries.

Nuno M C MartinsWellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh EH9 3JR, Scotland, United Kingdom.
Jan H BergmannWellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh EH9 3JR, Scotland, United Kingdom.
Nobuaki ShonoLaboratory of Cell Engineering, Department of Frontier Research, Kazusa DNA Research Institute, Kisarazu 292-0818, Japan Division of Biological Science, Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan.
Hiroshi KimuraGraduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama 226-8501, Japan.
Vladimir LarionovLaboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Hiroshi MasumotoLaboratory of Cell Engineering, Department of Frontier Research, Kazusa DNA Research Institute, Kisarazu 292-0818, Japan.
William C EarnshawWellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh EH9 3JR, Scotland, United Kingdom bill.earnshaw@ed.ac.uk.
Wellcome Centre for Cell Biology · GBKazusa DNA Research Institute · JPNational Institutes of Health · USTokyo Institute of Technology · JP

Funding

Intramural NIH HHSWellcome Trust 073915Wellcome Trust 077707Wellcome Trust 080458Wellcome Trust 092076Wellcome Trust 107022
6 · The paper itself

Abstract

Centromeres are characterized by the centromere-specific H3 variant CENP-A, which is embedded in chromatin with a pattern characteristic of active transcription that is required for centromere identity. It is unclear how centromeres remain transcriptionally active despite being flanked by repressive pericentric heterochromatin. To further understand centrochromatin's response to repressive signals, we nucleated a Polycomb-like chromatin state within the centromere of a human artificial chromosome (HAC) by tethering the methyltransferase EZH2. This led to deposition of the H3K27me3 mark and PRC1 repressor binding. Surprisingly, this state did not abolish HAC centromere function or transcription, and this apparent resistance was not observed on a noncentromeric locus, where transcription was silenced. Directly tethering the reader/repressor PRC1 bypassed this resistance, inactivating the centromere. We observed analogous responses when tethering the heterochromatin Editor Suv39h1-methyltransferase domain (centromere resistance) or reader HP1α (centromere inactivation), respectively. Our results reveal that the HAC centromere can resist repressive pathways driven by H3K9me3/H3K27me3 and may help to explain how centromeres are able to resist inactivation by flanking heterochromatin.

Indexed as

Cell Cycle ProteinsCells, CulturedCentromereChromatinChromobox Protein Homolog 5Chromosomes, Artificial, HumanEnhancer of Zeste Homolog 2 ProteinEpigenesis, GeneticEpigenomicsHeLa CellsHeterochromatinHistonesHumansKinetochoresMethyltransferasesPolycomb Repressive Complex 2CBX5 protein, humanCell Cycle ProteinsChromatinChromobox Protein Homolog 5Enhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHeterochromatinHistonesMethyltransferasesPolycomb Repressive Complex 2PRC1 protein, human

Identifiers

PMID26564795
PMCPMC4694756
OpenAlexW2308524041

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.