Evidence map›Paper›PMID 25047840›Full record

ArticleMolecular and cellular biology2014

Polycomb repressive complex 2 and H3K27me3 cooperate with H3K9 methylation to maintain heterochromatin protein 1α at chromatin.

Joanna Boros, Nausica Arnoult, Vincent Stroobant, Jean-François Collet, Anabelle Decottignies

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
5.1field-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

72 citing papers in PubMed, 137 citations in OpenAlex.

  1. Review
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  6. Physical models reveal indirect reader protein interactions that facilitate epigenetic crosstalk.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  12. Establishment and Maintenance of Heat-Stress Memory in Plants.International journal of molecular sciences · 2024
    Review
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  15. Functional analyses of the polycomb-group genes in sea lamprey embryos undergoing programmed DNA loss.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2024
    Article
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  18. Review
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12 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

Joanna BorosGenetic and Epigenetic Alterations of Genomes, de Duve Institute, Catholic University of Louvain, Brussels, Belgium.
Nausica ArnoultGenetic and Epigenetic Alterations of Genomes, de Duve Institute, Catholic University of Louvain, Brussels, Belgium.
Vincent StroobantLudwig Institute for Cancer Research, Brussels Branch, and de Duve Institute, Catholic University of Louvain, Brussels, Belgium.
Jean-François ColletWELBIO and de Duve Institute, Catholic University of Louvain, Brussels, Belgium.
Anabelle DecottigniesGenetic and Epigenetic Alterations of Genomes, de Duve Institute, Catholic University of Louvain, Brussels, Belgium anabelle.decottignies@uclouvain.be.
de Duve Institute · BEUCLouvain · BELudwig Cancer Research · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methylation of histone H3 on lysine 9 or 27 is crucial for heterochromatin formation. Previously considered hallmarks of, respectively, constitutive and facultative heterochromatin, recent evidence has accumulated in favor of coexistence of these two marks and their cooperation in gene silencing maintenance. H3K9me2/3 ensures anchorage at chromatin of heterochromatin protein 1α (HP1α), a main component of heterochromatin. HP1α chromoshadow domain, involved in dimerization and interaction with partners, has additional but still unclear roles in HP1α recruitment to chromatin. Because of previously suggested links between polycomb repressive complex 2 (PRC2), which catalyzes H3K27 methylation, and HP1α, we tested whether PRC2 may regulate HP1α abundance at chromatin. We found that the EZH2 and SUZ12 subunits of PRC2 are required for HP1α stability, as knockdown of either protein led to HP1α degradation. Similar results were obtained upon overexpression of H3K27me2/3 demethylases. We further showed that binding of HP1α/β/γ to H3K9me3 peptides is greatly increased in the presence of H3K27me3, and this is dependent on PRC2. These data fit with recent proteomic studies identifying PRC2 as an indirect H3K9me3 binder in mouse tissues and suggest the existence of a cooperative mechanism of HP1α anchorage at chromatin involving H3 methylation on both K9 and K27 residues.

Indexed as

AnimalsCell CycleCell Line, TumorChromatinChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneHistonesHumansMethylationMiceModels, MolecularNeoplasmsPolycomb Repressive Complex 2Proteasome Endopeptidase ComplexProtein StabilityCBX5 protein, humanChromatinChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneHistonesPolycomb Repressive Complex 2Proteasome Endopeptidase Complex

Identifiers

PMID25047840
PMCPMC4187721
OpenAlexW2110628320

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.