Evidence map›Paper›PMID 36064597›Full record

ArticleNature structural & molecular biology2022

Histone deacetylation primes self-propagation of heterochromatin domains to promote epigenetic inheritance.

Martin Zofall, Rima Sandhu, Sahana Holla, David Wheeler, Shiv I S Grewal

Open access · greenAbstract read
In one paragraph

Article in Nature structural & molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  7. HISTONE DEACETYLASE-1 is required for epigenome stability inProceedings of the National Academy of Sciences of the United States of America · 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

5 authors at 1 institution in 1 country.

Martin ZofallLaboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Rima SandhuLaboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Sahana HollaLaboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
David WheelerLaboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0002-2929-4204
Shiv I S GrewalLaboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. grewals@mail.nih.gov.ORCID http://orcid.org/0000-0002-4552-9261
National Institutes of Health · US

Funding

Roles of Chromatin-modifying Factors in Epigenetic Control of the GenomeZIABC011208 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GREWAL, SHIVINDER S · 2009 to 2025
$28.1M
Intramural NIH HHS ZIA BC011208
6 · The paper itself

Abstract

Heterochromatin assembly, involving histone H3 lysine-9 methylation (H3K9me), is nucleated at specific genomic sites but can self-propagate across extended domains and, indeed, generations. Self-propagation requires Clr4/Suv39h methyltransferase recruitment by pre-existing H3K9 tri-methylation (H3K9me3) to perpetuate H3K9me deposition and is dramatically affected by chromatin context. However, the mechanism priming self-propagation of heterochromatin remains undefined. We show that robust chromatin association of fission yeast class II histone deacetylase Clr3 is necessary and sufficient to support heterochromatin propagation in different chromosomal contexts. Efficient targeting of Clr3, which suppresses histone turnover and maintains H3K9me3, enables self-propagation of an ectopic heterochromatin domain via the Clr4/Suv39h read-write mechanism requiring methylated histones. The deacetylase activity of Clr3 is necessary and, when inactivated, heterochromatin propagation can be recapitulated by removing two major histone acetyltransferases. Our results show that histone deacetylation, a conserved heterochromatin feature, preserves H3K9me3 that transmits epigenetic memory for stable propagation of silenced chromatin domains through multiple generations.

Indexed as

SchizosaccharomycesSchizosaccharomyces pombe ProteinsCell Cycle ProteinsEpigenesis, GeneticHeterochromatinHistone AcetyltransferasesHistone DeacetylasesHistone-Lysine N-MethyltransferaseHistonesLysineCell Cycle Proteinsclr4 protein, S pombeHeterochromatinHistone AcetyltransferasesHistone DeacetylasesHistone-Lysine N-MethyltransferaseHistonesLysineSchizosaccharomyces pombe Proteins

Identifiers

PMID36064597
PMCPMC10357965
OpenAlexW4294636947

What OpenQuestion holds

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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.