Evidence map›Paper›PMID 35081363›Full record

ArticleMolecular cell2022

SETDB1/NSD-dependent H3K9me3/H3K36me3 dual heterochromatin maintains gene expression profiles by bookmarking poised enhancers.

Amandine Barral, Gabrielle Pozo, Lucas Ducrot, Giorgio L Papadopoulos, Sandrine Sauzet, Andrew J Oldfield, Giacomo Cavalli, Jérôme Déjardin

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. The Many Faces of SetDB1.Epigenomes · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Epigenetic remodeling during early embryonic development.Frontiers in cell and developmental biology · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

8 authors at 1 institution in 1 country.

Amandine BarralDNA Repeat Lab, Institute of Human Genetics CNRS-Université de Montpellier UMR 9002, 141 rue de la Cardonille, 34000 Montpellier, France.
Gabrielle PozoDNA Repeat Lab, Institute of Human Genetics CNRS-Université de Montpellier UMR 9002, 141 rue de la Cardonille, 34000 Montpellier, France.
Lucas DucrotDNA Repeat Lab, Institute of Human Genetics CNRS-Université de Montpellier UMR 9002, 141 rue de la Cardonille, 34000 Montpellier, France.
Giorgio L PapadopoulosChromatin and Cell Biology Lab, Institute of Human Genetics CNRS-Université de Montpellier UMR 9002, 141 rue de la Cardonille, 34000 Montpellier, France.
Sandrine SauzetDNA Repeat Lab, Institute of Human Genetics CNRS-Université de Montpellier UMR 9002, 141 rue de la Cardonille, 34000 Montpellier, France.
Andrew J OldfieldChromatin and Splicing Lab, Institute of Human Genetics CNRS-Université de Montpellier UMR 9002, 141 rue de la Cardonille, 34000 Montpellier, France.
Giacomo CavalliChromatin and Cell Biology Lab, Institute of Human Genetics CNRS-Université de Montpellier UMR 9002, 141 rue de la Cardonille, 34000 Montpellier, France.
Jérôme DéjardinDNA Repeat Lab, Institute of Human Genetics CNRS-Université de Montpellier UMR 9002, 141 rue de la Cardonille, 34000 Montpellier, France. Electronic address: jerome.dejardin@igh.cnrs.fr.
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene silencing by heterochromatin plays a crucial role in cell identity. Here, we characterize the localization, the biogenesis, and the function of an atypical heterochromatin, which is simultaneously enriched in the typical H3K9me3 mark and in H3K36me3, a histone mark usually associated with gene expression. We identified thousands of dual regions in mouse embryonic stem (ES) cells that rely on the histone methyltransferases SET domain bifurcated 1 (SETDB1) and nuclear set domain (NSD)-containing proteins to generate H3K9me3 and H3K36me3, respectively. Upon SETDB1 removal, dual domains lose both marks, gain signatures of active enhancers, and come into contact with upregulated genes, suggesting that it might be an important pathway by which genes are controlled by heterochromatin. In differentiated tissues, a subset of these dual domains is destabilized and becomes enriched in active enhancer marks, providing a mechanistic insight into the involvement of heterochromatin in the maintenance of cell identity.

Indexed as

Chromatin Assembly and DisassemblyDNA MethylationEnhancer Elements, GeneticProtein Processing, Post-TranslationalAnimalsCell LineChromatin Immunoprecipitation SequencingGene Expression ProfilingGene Expression Regulation, DevelopmentalHeterochromatinHistone-Lysine N-MethyltransferaseHistonesMethylationMiceMouse Embryonic Stem CellsRNA-SeqHeterochromatinHistone-Lysine N-MethyltransferaseHistonesNsd1 protein, mouseSETD2 protein, mouseSETDB1 protein, mouseWHSC1L1 protein, mouseWHSC1 protein, mousecellular identityenhancergene expressionheterochromatin

Identifiers

PMID35081363
PMCPMC8860380
OpenAlexW4206898670

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.