Evidence map›Paper›PMID 34737442›Full record

ArticleNature cell biology2021

H3K9me selectively blocks transcription factor activity and ensures differentiated tissue integrity.

Stephen P Methot, Jan Padeken, Giovanna Brancati, Peter Zeller, Colin E Delaney, Dimos Gaidatzis, Hubertus Kohler, Alexander van Oudenaarden, Helge Großhans, Susan M Gasser

Open access · hybridAbstract read
In one paragraph

Article in Nature cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.6field-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

54 citing papers in PubMed, 76 citations in OpenAlex.

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  12. Lactate Enhances CD8International journal of molecular sciences · 2026
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  13. Epigenetic constraints and enhancer innovation link neuronal plasticity to evolutionary adaptation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

10 authors at 5 institutions in 2 countries.

Stephen P Methot *Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland.ORCID http://orcid.org/0000-0003-2854-2226
Jan Padeken *Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Giovanna BrancatiFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Peter ZellerHubrecht Institute-KNAW and University Medical Center, Utrecht, The Netherlands.
Colin E DelaneyFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.ORCID http://orcid.org/0000-0001-6880-6973
Dimos GaidatzisFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Hubertus KohlerFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Alexander van OudenaardenHubrecht Institute-KNAW and University Medical Center, Utrecht, The Netherlands.ORCID http://orcid.org/0000-0002-9442-3551
Helge GroßhansFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.ORCID http://orcid.org/0000-0002-8169-6905
Susan M GasserFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland. susan.gasser@fmi.ch.ORCID http://orcid.org/0000-0003-3610-9123
Friedrich Miescher Institute · CHUniversity Medical Center Utrecht · NLUniversity of Basel · CHETH Zurich · CHSIB Swiss Institute of Bioinformatics · CH

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
NIH HHS P40 OD010440
6 · The paper itself

Abstract

The developmental role of histone H3K9 methylation (H3K9me), which typifies heterochromatin, remains unclear. In Caenorhabditis elegans, loss of H3K9me leads to a highly divergent upregulation of genes with tissue and developmental-stage specificity. During development H3K9me is lost from differentiated cell type-specific genes and gained at genes expressed in earlier developmental stages or other tissues. The continuous deposition of H3K9me2 by the SETDB1 homolog MET-2 after terminal differentiation is necessary to maintain repression. In differentiated tissues, H3K9me ensures silencing by restricting the activity of a defined set of transcription factors at promoters and enhancers. Increased chromatin accessibility following the loss of H3K9me is neither sufficient nor necessary to drive transcription. Increased ATAC-seq signal and gene expression correlate at a subset of loci positioned away from the nuclear envelope, while derepressed genes at the nuclear periphery remain poorly accessible despite being transcribed. In conclusion, H3K9me deposition can confer tissue-specific gene expression and maintain the integrity of terminally differentiated muscle by restricting transcription factor activity.

Indexed as

Cell DifferentiationChromatin Assembly and DisassemblyProtein Processing, Post-TranslationalTranscription, GeneticAnimalsAnimals, Genetically ModifiedBinding SitesCaenorhabditis elegansCaenorhabditis elegans ProteinsChromatin Immunoprecipitation SequencingGene Expression ProfilingHistone-Lysine N-MethyltransferaseHistonesMethylationProtein BindingTime FactorsCaenorhabditis elegans ProteinsHistone-Lysine N-MethyltransferaseHistonesMet-2 protein, C elegans

Identifiers

PMID34737442
PMCPMC8572725
OpenAlexW3208823525

What OpenQuestion holds

Textmetadata
LicenceTDM
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.