Evidence map›Paper›PMID 39096900›Full record

ArticleMolecular cell2024

Nucleosome remodeler exclusion by histone deacetylation enforces heterochromatic silencing and epigenetic inheritance.

Rakesh Kumar Sahu, Jothy Dhakshnamoorthy, Shweta Jain, Hernan Diego Folco, David Wheeler, Shiv I S Grewal

Abstract read
In one paragraph

Article in Molecular cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

  1. Review
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  8. Balkan medical journal · 2026
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. HISTONE DEACETYLASE-1 is required for epigenome stability inProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  15. Review
  16. Article
  17. Fto-mediated mJournal of biomedical science · 2025
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Rakesh Kumar SahuLaboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Jothy DhakshnamoorthyLaboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Shweta JainLaboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Hernan Diego FolcoLaboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
David WheelerLaboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Shiv I S GrewalLaboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: grewals@mail.nih.gov.

Funding

RNAi and Epigenetic Control of Higher-Order Chromatin AssemblyZIABC010523 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GREWAL, SHIVINDER S · 2009 to 2025
$28.1M
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
RNAi and Epigenetic Control of Higher-Order Chromatin AssemblyZ01BC010523 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GREWAL, SHIVINDER S · 2003 to 2008
$4.4M
Intramural NIH HHS Z01 BC010523Intramural NIH HHS Z99 CA999999Intramural NIH HHS ZIA BC010523Intramural NIH HHS ZIA BC011208
6 · The paper itself

Abstract

Heterochromatin enforces transcriptional gene silencing and can be epigenetically inherited, but the underlying mechanisms remain unclear. Here, we show that histone deacetylation, a conserved feature of heterochromatin domains, blocks SWI/SNF subfamily remodelers involved in chromatin unraveling, thereby stabilizing modified nucleosomes that preserve gene silencing. Histone hyperacetylation, resulting from either the loss of histone deacetylase (HDAC) activity or the direct targeting of a histone acetyltransferase to heterochromatin, permits remodeler access, leading to silencing defects. The requirement for HDAC in heterochromatin silencing can be bypassed by impeding SWI/SNF activity. Highlighting the crucial role of remodelers, merely targeting SWI/SNF to heterochromatin, even in cells with functional HDAC, increases nucleosome turnover, causing defective gene silencing and compromised epigenetic inheritance. This study elucidates a fundamental mechanism whereby histone hypoacetylation, maintained by high HDAC levels in heterochromatic regions, ensures stable gene silencing and epigenetic inheritance, providing insights into genome regulatory mechanisms relevant to human diseases.

Indexed as

Chromatin Assembly and DisassemblyEpigenesis, GeneticGene SilencingHeterochromatinHistone DeacetylasesHistonesNucleosomesAcetylationAnimalsHistone AcetyltransferasesHumansHeterochromatinHistone AcetyltransferasesHistone DeacetylasesHistonesNucleosomeschromatin remodelingepigenetic inheritancegene silencingH3K9me3heterochromatinhistone deacetylationhistone modificationsread-writeRSCSWI/SNF

Identifiers

PMID39096900
PMCPMC11649001

What Socratic 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 Socratic graph.