Evidence map›Paper›PMID 40696106›Full record

ArticleNature cell biology2025

The nuclear periphery confers repression on H3K9me2-marked genes and transposons to shape cell fate.

Harold C Marin, Charlie Allen, Eric Simental, Eric W Martin, Barbara Panning, Bassem Al-Sady, Abigail Buchwalter

Abstract read
In one paragraph

Article in Nature cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Review
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  6. Review
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  8. A Translocation within thebioRxiv : the preprint server for biology · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Nucleoskeletal Proteins in Early Embryogenesis.Advances in experimental medicine and biology · 2026
    Review
  15. Article
  16. Article
  17. Article
  18. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Harold C MarinCardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA.
Charlie Allen *Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA.
Eric Simental *Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA, USA.
Eric W MartinCardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA.
Barbara PanningDepartment of Biochemistry, University of California, San Francisco, San Francisco, CA, USA.
Bassem Al-SadyDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA, USA.
Abigail BuchwalterCardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA. abigail.buchwalter@ucsf.edu.ORCID http://orcid.org/0000-0001-7181-6961

Funding

UCSF IRACDA Scholars ProgramK12GM081266 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Raymond M. Esquerra, HOLLY A. INGRAHAM · 2007 to 2026
$19.4M
MOLECULAR AND CELLULAR BASIS OF CARDIOVASCULAR DISEASET32HL007731 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Brian L Black · 1992 to 2026
$12.4M
Understanding mechanisms of heterochromatin tethering at the nuclear laminaR35GM142897 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Abigail Lynn Buchwalter · 2021 to 2026
$2.4M
Tracking how molecular machines propagate epigenetic information in time and spaceR35GM141888 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI AL-SADY, BASSEM · 2021 to 2025
$2.3M
OneView 4kX4k sCMOS camera for transmission electron microscopy applicationsS10OD028536 · OD · STANFORD UNIVERSITY · PI MULHOLLAND, JONATHAN W · 2020 to 2020
$195k
NHLBI NIH HHS T32 HL007731NIGMS NIH HHS K12 GM081266NIGMS NIH HHS R35 GM141888NIGMS NIH HHS R35 GM142897NIH HHS S10 OD028536U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R35GM141888U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R35GM142897
6 · The paper itself

Abstract

Heterochromatic loci marked by histone H3 lysine 9 dimethylation (H3K9me2) are enriched at the nuclear periphery in metazoans, but the effect of spatial position on heterochromatin function has not been defined. Here we remove three nuclear lamins and the lamin B receptor (LBR) in mouse embryonic stem cells and show that heterochromatin detaches from the nuclear periphery. Mutant mouse embryonic stem cells sustain naive pluripotency and maintain H3K9me2 across the genome but cannot repress H3K9me2-marked genes or transposons. Further, mutant cells fail to differentiate into epiblast-like cells, a transition that requires the expansion of H3K9me2 across the genome. Mutant epiblast-like cells can silence naive pluripotency genes and activate epiblast-stage genes. However, H3K9me2 cannot repress markers of alternative fates, including primitive endoderm. We conclude that the lamins and LBR control the spatial position, dynamic remodelling and repressive capacity of H3K9me2-marked heterochromatin to shape cell fate decisions.

Indexed as

Cell NucleusCell ShapeDNA Transposable ElementsHeterochromatinHistonesMouse Embryonic Stem CellsAnimalsDNA-Binding ProteinsGene Expression Regulation, DevelopmentalGene Knockout TechniquesGenomeGerm LayersHistone CodeLamin B ReceptorLaminsMembrane ProteinsDNA-Binding ProteinsDNA Transposable ElementsHeterochromatinHistoneslamina-associated polypeptide 2Lamin B ReceptorLaminsLbr protein, mouseMembrane Proteins

Identifiers

PMID40696106
PMCPMC12339402

What OpenQuestion holds

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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.