Evidence map›Paper›PMID 35102319›Full record

ArticleNature structural & molecular biology2022

SETDB1-like MET-2 promotes transcriptional silencing and development independently of its H3K9me-associated catalytic activity.

Colin E Delaney, Stephen P Methot, Veronique Kalck, Jan Seebacher, Daniel Hess, Susan M Gasser, Jan Padeken

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Nature structural & molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. The Many Faces of SetDB1.Epigenomes · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. 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
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. SetDB1 and Su(var)3-9 are essential for late stages of larval development of Drosophila melanogaster.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023
    Article
  15. SETDB1 regulates microtubule dynamics.Cell proliferation · 2022
    Article
  16. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Colin E DelaneyFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.ORCID http://orcid.org/0000-0001-6880-6973
Stephen P MethotFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.ORCID http://orcid.org/0000-0003-2854-2226
Veronique KalckFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Jan SeebacherFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.ORCID http://orcid.org/0000-0002-7858-2720
Daniel HessFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.ORCID http://orcid.org/0000-0002-1642-5404
Susan M GasserFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland. susan.gasser@fmi.ch.ORCID http://orcid.org/0000-0003-3610-9123
Jan PadekenFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Friedrich Miescher Institute · CHUniversity of Basel · CH

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
NIH HHS P40 OD010440
6 · The paper itself

Abstract

Transcriptionally silenced heterochromatin bearing methylation of histone H3 on lysine 9 (H3K9me) is critical for maintaining organismal viability and tissue integrity. Here we show that in addition to ensuring H3K9me, MET-2, the Caenorhabditis elegans homolog of the SETDB1 histone methyltransferase, has a noncatalytic function that contributes to gene repression. Subnuclear foci of MET-2 coincide with H3K9me deposition, yet these foci also form when MET-2 is catalytically deficient and H3K9me is compromised. Whereas met-2 deletion triggers a loss of silencing and increased histone acetylation, foci of catalytically deficient MET-2 maintain silencing of a subset of genes, blocking acetylation on H3K9 and H3K27. In normal development, this noncatalytic MET-2 activity helps to maintain fertility. Under heat stress MET-2 foci disperse, coinciding with increased acetylation and transcriptional derepression. Our study suggests that the noncatalytic, focus-forming function of this SETDB1-like protein and its intrinsically disordered cofactor LIN-61 is physiologically relevant.

Indexed as

AnimalsAnimals, Genetically ModifiedBiocatalysisCaenorhabditis elegansCaenorhabditis elegans ProteinsChromosomal Proteins, Non-HistoneGene SilencingHeterochromatinHistone-Lysine N-MethyltransferaseHistonesIntrinsically Disordered ProteinsMethylationModels, BiologicalMutationTranscription, GeneticCaenorhabditis elegans ProteinsChromosomal Proteins, Non-HistoneHeterochromatinHistone-Lysine N-MethyltransferaseHistonesIntrinsically Disordered ProteinsLIN-61 protein, C elegansMet-2 protein, C elegans

Identifiers

PMID35102319
PMCPMC8850192
OpenAlexW4210672529

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.