Evidence map›Paper›PMID 35776115›Full record

ArticleNucleic acids research2022

SETDB1 acts as a topological accessory to Cohesin via an H3K9me3-independent, genomic shunt for regulating cell fates.

Tushar Warrier, Chadi El Farran, Yingying Zeng, Benedict Shao Quan Ho, Qiuye Bao, Zi Hao Zheng, Xuezhi Bi, Huck Hui Ng, Derrick Sek Tong Ong, Justin Jang Hann Chu and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 33 citations in OpenAlex.

  1. The Many Faces of SetDB1.Epigenomes · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. SETDB1 ensures the continuity of embryonic to adult neural stem cells through metabolic alterations in the dentate gyrus.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Setdb1 ablation in macrophages attenuates fibrosis in heart allografts.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Histone methyltransferase SETDB1 safeguards mouse fetal hematopoiesis by suppressing activation of cryptic enhancers.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Article
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  20. Review
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

16 authors at 7 institutions in 3 countries.

Tushar WarrierCell Fate Engineering and Therapeutics Lab, Cell Biology and Therapies Division, A*STAR Institute of Molecular and Cell Biology, Singapore 138673, Singapore.ORCID 0000-0003-4839-5067
Chadi El FarranCell Fate Engineering and Therapeutics Lab, Cell Biology and Therapies Division, A*STAR Institute of Molecular and Cell Biology, Singapore 138673, Singapore.ORCID 0000-0002-9374-103X
Yingying ZengCell Fate Engineering and Therapeutics Lab, Cell Biology and Therapies Division, A*STAR Institute of Molecular and Cell Biology, Singapore 138673, Singapore.
Benedict Shao Quan HoCell Fate Engineering and Therapeutics Lab, Cell Biology and Therapies Division, A*STAR Institute of Molecular and Cell Biology, Singapore 138673, Singapore.
Qiuye BaoCell Fate Engineering and Therapeutics Lab, Cell Biology and Therapies Division, A*STAR Institute of Molecular and Cell Biology, Singapore 138673, Singapore.
Zi Hao ZhengCell Fate Engineering and Therapeutics Lab, Cell Biology and Therapies Division, A*STAR Institute of Molecular and Cell Biology, Singapore 138673, Singapore.
Xuezhi BiProteomics Group, Bioprocessing Technology Institute, A*STAR, Singapore 138668, Singapore.ORCID 0000-0001-6702-0805
Huck Hui NgGene Regulation Laboratory, Genome Institute of Singapore, Singapore 138672, Singapore.
Derrick Sek Tong OngDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117593, Singapore.
Justin Jang Hann ChuDepartment of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117593, Singapore.
Amartya SanyalSchool of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive 637551, Singapore.
Melissa Jane FullwoodSchool of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive 637551, Singapore.
James J CollinsHoward Hughes Medical Institute, Boston, MA 02114, USA.
Hu LiCenter for Individualized Medicine, Department of Molecular Pharmacology & Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905, USA.
Jian XuDepartment of Biological Sciences, National University of Singapore, Singapore 117543, Singapore.
Yuin-Han LohCell Fate Engineering and Therapeutics Lab, Cell Biology and Therapies Division, A*STAR Institute of Molecular and Cell Biology, Singapore 138673, Singapore.
Agency for Science, Technology and Research · SGNational University of Singapore · SGBroad Institute · USGenome Institute of Singapore · SGMayo Clinic · USNanyang Technological University · SGRadboud University Nijmegen · NL

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI AKHILESH PANDEY · 1985 to 2026
$151.3M
Capturing the molecular complexity of Alzheimer's disease through the lens of RNA binding proteinsRF1AG056318 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LI, HU, WOLOZIN, BENJAMIN L · 2018 to 2020
$4.4M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA015083NIA NIH HHS RF1 AG056318
6 · The paper itself

Abstract

SETDB1 is a key regulator of lineage-specific genes and endogenous retroviral elements (ERVs) through its deposition of repressive H3K9me3 mark. Apart from its H3K9me3 regulatory role, SETDB1 has seldom been studied in terms of its other potential regulatory roles. To investigate this, a genomic survey of SETDB1 binding in mouse embryonic stem cells across multiple libraries was conducted, leading to the unexpected discovery of regions bereft of common repressive histone marks (H3K9me3, H3K27me3). These regions were enriched with the CTCF motif that is often associated with the topological regulator Cohesin. Further profiling of these non-H3K9me3 regions led to the discovery of a cluster of non-repeat loci that were co-bound by SETDB1 and Cohesin. These regions, which we named DiSCs (domains involving SETDB1 and Cohesin) were seen to be proximal to the gene promoters involved in embryonic stem cell pluripotency and lineage development. Importantly, it was found that SETDB1-Cohesin co-regulate target gene expression and genome topology at these DiSCs. Depletion of SETDB1 led to localized dysregulation of Cohesin binding thereby locally disrupting topological structures. Dysregulated gene expression trends revealed the importance of this cluster in ES cell maintenance as well as at gene 'islands' that drive differentiation to other lineages. The 'unearthing' of the DiSCs thus unravels a unique topological and transcriptional axis of control regulated chiefly by SETDB1.

Indexed as

Endogenous RetrovirusesHistonesAnimalsCell Cycle ProteinsChromosomal Proteins, Non-HistoneCohesinsGenomicsHistone-Lysine N-MethyltransferaseMiceCell Cycle ProteinsChromosomal Proteins, Non-HistoneCohesinsHistone-Lysine N-MethyltransferaseHistonesSETDB1 protein, mouse

Identifiers

PMID35776115
PMCPMC9303280
OpenAlexW4283766509

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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.