Evidence map›Paper›PMID 33514712›Full record

ArticleNature communications2021

H3K27me3-rich genomic regions can function as silencers to repress gene expression via chromatin interactions.

Yichao Cai, Ying Zhang, Yan Ping Loh, Jia Qi Tng, Mei Chee Lim, Zhendong Cao, Anandhkumar Raju, Erez Lieberman Aiden, Shang Li, Lakshmanan Manikandan and 3 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 192 papers.

0numbers the graph read from it
0cells of the map it votes in
192citing papers in PubMed
19.7field-weighted citation impact, top 1% 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

192 citing papers in PubMed, 319 citations in OpenAlex.

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  7. Palmitic Acid Amplifies Microglial Inflammatory Activation Involving C5aR1-Sensitive Inflammatory Signaling and JMJD3/H3K27me3-Related Epigenetic Changes.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article
  8. The Encyclopedia of DNA Elements.bioRxiv : the preprint server for biology · 2026
    Article
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132 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

13 authors at 3 institutions in 3 countries.

Yichao Cai *Cancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.ORCID 0000-0002-5142-4167
Ying Zhang *Cancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Yan Ping LohCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Jia Qi TngCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Mei Chee LimCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.ORCID 0000-0002-8338-9554
Zhendong CaoCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Anandhkumar RajuInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Proteos, Singapore.
Erez Lieberman AidenDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Shang LiCancer and Stem Cell Biology Programme, Duke-NUS Medical School, Singapore, Singapore.
Lakshmanan ManikandanInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Proteos, Singapore.
Vinay TergaonkarInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Proteos, Singapore.
Greg Tucker-KelloggDepartment of Biological Sciences, National University of Singapore, Singapore, Singapore. dbsgtk@nus.edu.sg.ORCID 0000-0001-8407-9251
Melissa Jane FullwoodCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore. mfullwood@ntu.edu.sg.ORCID 0000-0003-0321-7865
National University of Singapore · SGAgency for Science, Technology and Research · SGBaylor College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms underlying gene repression and silencers are poorly understood. Here we investigate the hypothesis that H3K27me3-rich regions of the genome, defined from clusters of H3K27me3 peaks, may be used to identify silencers that can regulate gene expression via proximity or looping. We find that H3K27me3-rich regions are associated with chromatin interactions and interact preferentially with each other. H3K27me3-rich regions component removal at interaction anchors by CRISPR leads to upregulation of interacting target genes, altered H3K27me3 and H3K27ac levels at interacting regions, and altered chromatin interactions. Chromatin interactions did not change at regions with high H3K27me3, but regions with low H3K27me3 and high H3K27ac levels showed changes in chromatin interactions. Cells with H3K27me3-rich regions knockout also show changes in phenotype associated with cell identity, and altered xenograft tumor growth. Finally, we observe that H3K27me3-rich regions-associated genes and long-range chromatin interactions are susceptible to H3K27me3 depletion. Our results characterize H3K27me3-rich regions and their mechanisms of functioning via looping.

Indexed as

Epigenetic RepressionAnimalsCell Line, TumorChromatinChromatin Immunoprecipitation SequencingFemaleFibroblast Growth FactorsGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene Knockout TechniquesHistonesHumansInsulin-Like Growth Factor IIMiceNeoplasmsRNA-SeqChromatinfibroblast growth factor 18Fibroblast Growth FactorsHistonesIGF2 protein, humanInsulin-Like Growth Factor II

Identifiers

PMID33514712
PMCPMC7846766
OpenAlexW3124680305

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.