Evidence map›Paper›PMID 34272378›Full record

ArticleNature communications2021

Complete loss of H3K9 methylation dissolves mouse heterochromatin organization.

Thomas Montavon, Nicholas Shukeir, Galina Erikson, Bettina Engist, Megumi Onishi-Seebacher, Devon Ryan, Yaarub Musa, Gerhard Mittler, Alexandra Graff Meyer, Christel Genoud and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

79 citing papers in PubMed, 105 citations in OpenAlex.

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  18. Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025
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19 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

11 authors at 5 institutions in 2 countries.

Thomas MontavonMax-Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.ORCID 0000-0001-8247-1399
Nicholas ShukeirMax-Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
Galina EriksonMax-Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
Bettina EngistMax-Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
Megumi Onishi-SeebacherMax-Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
Devon RyanMax-Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
Yaarub MusaMax-Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
Gerhard MittlerMax-Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
Alexandra Graff MeyerFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Christel GenoudFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Thomas JenuweinMax-Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany. jenuwein@ie-freiburg.mpg.de.ORCID 0000-0002-0470-0421
Max Planck Institute of Immunobiology and Epigenetics · DEFriedrich Miescher Institute · CHGenedata (Switzerland) · CHNovartis (Switzerland) · CHThermo Fisher Scientific (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone H3 lysine 9 (H3K9) methylation is a central epigenetic modification that defines heterochromatin from unicellular to multicellular organisms. In mammalian cells, H3K9 methylation can be catalyzed by at least six distinct SET domain enzymes: Suv39h1/Suv39h2, Eset1/Eset2 and G9a/Glp. We used mouse embryonic fibroblasts (MEFs) with a conditional mutation for Eset1 and introduced progressive deletions for the other SET domain genes by CRISPR/Cas9 technology. Compound mutant MEFs for all six SET domain lysine methyltransferase (KMT) genes lack all H3K9 methylation states, derepress nearly all families of repeat elements and display genomic instabilities. Strikingly, the 6KO H3K9 KMT MEF cells no longer maintain heterochromatin organization and have lost electron-dense heterochromatin. This is a compelling analysis of H3K9 methylation-deficient mammalian chromatin and reveals a definitive function for H3K9 methylation in protecting heterochromatin organization and genome integrity.

Indexed as

AnimalsChromatin Immunoprecipitation SequencingChromatography, LiquidCRISPR-Cas SystemsDemethylationEpigenesis, GeneticFibroblastsGene DeletionHeterochromatinHistone-Lysine N-MethyltransferaseHistonesIn Situ Hybridization, FluorescenceLysineMass SpectrometryMethylationMiceHeterochromatinHistone-Lysine N-MethyltransferaseHistonesLysineRetroelementsSETDB1 protein, mouse

Identifiers

PMID34272378
PMCPMC8285382
OpenAlexW3178521824

What OpenQuestion holds

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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.