Evidence map›Paper›PMID 36123357›Full record

ArticleNature communications2022

Dominant role of DNA methylation over H3K9me3 for IAP silencing in endoderm.

Zeyang Wang, Rui Fan, Angela Russo, Filippo M Cernilogar, Alexander Nuber, Silvia Schirge, Irina Shcherbakova, Iva Dzhilyanova, Enes Ugur, Tobias Anton and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  12. Reversing transgene silencing via targeted chromatin editing.bioRxiv : the preprint server for biology · 2025
    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
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  18. Review
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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

14 authors at 4 institutions in 1 country.

Zeyang Wang *Division of Molecular Biology, Biomedical Center, Faculty of Medicine, LMU Munich, Munich, Germany.ORCID 0000-0001-5735-0675
Rui Fan *Division of Molecular Biology, Biomedical Center, Faculty of Medicine, LMU Munich, Munich, Germany.
Angela RussoDivision of Molecular Biology, Biomedical Center, Faculty of Medicine, LMU Munich, Munich, Germany.ORCID 0000-0001-8976-4055
Filippo M CernilogarDivision of Molecular Biology, Biomedical Center, Faculty of Medicine, LMU Munich, Munich, Germany.ORCID 0000-0003-2814-3436
Alexander NuberDivision of Molecular Biology, Biomedical Center, Faculty of Medicine, LMU Munich, Munich, Germany.
Silvia SchirgeHelmholtz Zentrum München, Institute of Stem Cell Research, Neuherberg, Germany.
Irina ShcherbakovaDivision of Molecular Biology, Biomedical Center, Faculty of Medicine, LMU Munich, Munich, Germany.
Iva DzhilyanovaDivision of Molecular Biology, Biomedical Center, Faculty of Medicine, LMU Munich, Munich, Germany.ORCID 0000-0001-5863-4573
Enes UgurBiozentrum, LMU Munich, Munich, Germany.
Tobias AntonBiozentrum, LMU Munich, Munich, Germany.
Lisa RichterBiomedical Center (BMC), Core Facility Flow Cytometry, Faculty of Medicine, LMU Munich, Munich, Germany.ORCID 0000-0002-0769-619X
Heinrich LeonhardtBiozentrum, LMU Munich, Munich, Germany.ORCID 0000-0002-5086-6449
Heiko LickertHelmholtz Zentrum München, Institute of Stem Cell Research, Neuherberg, Germany.ORCID 0000-0002-4597-8825
Gunnar SchottaDivision of Molecular Biology, Biomedical Center, Faculty of Medicine, LMU Munich, Munich, Germany. gunnar.schotta@bmc.med.lmu.de.ORCID 0000-0003-4940-6135
Ludwig-Maximilians-Universität München · DEHelmholtz Zentrum München · DELMU Klinikum · DEMax Planck Institute for Molecular Biomedicine · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Silencing of endogenous retroviruses (ERVs) is largely mediated by repressive chromatin modifications H3K9me3 and DNA methylation. On ERVs, these modifications are mainly deposited by the histone methyltransferase Setdb1 and by the maintenance DNA methyltransferase Dnmt1. Knock-out of either Setdb1 or Dnmt1 leads to ERV de-repression in various cell types. However, it is currently not known if H3K9me3 and DNA methylation depend on each other for ERV silencing. Here we show that conditional knock-out of Setdb1 in mouse embryonic endoderm results in ERV de-repression in visceral endoderm (VE) descendants and does not occur in definitive endoderm (DE). Deletion of Setdb1 in VE progenitors results in loss of H3K9me3 and reduced DNA methylation of Intracisternal A-particle (IAP) elements, consistent with up-regulation of this ERV family. In DE, loss of Setdb1 does not affect H3K9me3 nor DNA methylation, suggesting Setdb1-independent pathways for maintaining these modifications. Importantly, Dnmt1 knock-out results in IAP de-repression in both visceral and definitive endoderm cells, while H3K9me3 is unaltered. Thus, our data suggest a dominant role of DNA methylation over H3K9me3 for IAP silencing in endoderm cells. Our findings suggest that Setdb1-meditated H3K9me3 is not sufficient for IAP silencing, but rather critical for maintaining high DNA methylation.

Indexed as

DNA MethylationEndogenous RetrovirusesAnimalsChromatinDNAEndodermHistone MethyltransferasesHistonesMiceChromatinDNAHistone MethyltransferasesHistones

Identifiers

PMID36123357
PMCPMC9485127
OpenAlexW4296351276

What OpenQuestion holds

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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.