Evidence map›Paper›PMID 26109049›Full record

ArticleGenes & development2015

DNA methylation restrains transposons from adopting a chromatin signature permissive for meiotic recombination.

Natasha Zamudio, Joan Barau, Aurélie Teissandier, Marius Walter, Maté Borsos, Nicolas Servant, Déborah Bourc'his

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing 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

124 citing papers in PubMed, 187 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Why recombination hotspots?PLoS genetics · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. SomaticiScience · 2025
    Article
  18. Polymorphic transposable elements contribute to variation in recombination landscapes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  19. Article
  20. Article

64 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

7 authors at 2 institutions in 1 country.

Natasha ZamudioUMR3215, CNRS, Paris 75005, France; U934, INSERM Institut Curie, Paris 75005, France;
Joan BarauUMR3215, CNRS, Paris 75005, France; U934, INSERM Institut Curie, Paris 75005, France;
Aurélie TeissandierUMR3215, CNRS, Paris 75005, France; U934, INSERM Institut Curie, Paris 75005, France; U900, INSERM, Paris 75005, France; Mines ParisTech, Institut Curie, Paris 75005, France.
Marius WalterUMR3215, CNRS, Paris 75005, France; U934, INSERM Institut Curie, Paris 75005, France;
Maté BorsosUMR3215, CNRS, Paris 75005, France; U934, INSERM Institut Curie, Paris 75005, France;
Nicolas ServantU900, INSERM, Paris 75005, France; Mines ParisTech, Institut Curie, Paris 75005, France.
Déborah Bourc'hisUMR3215, CNRS, Paris 75005, France; U934, INSERM Institut Curie, Paris 75005, France;
Centre National de la Recherche Scientifique · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA methylation is essential for protecting the mammalian germline against transposons. When DNA methylation-based transposon control is defective, meiotic chromosome pairing is consistently impaired during spermatogenesis: How and why meiosis is vulnerable to transposon activity is unknown. Using two DNA methylation-deficient backgrounds, the Dnmt3L and Miwi2 mutant mice, we reveal that DNA methylation is largely dispensable for silencing transposons before meiosis onset. After this, it becomes crucial to back up to a developmentally programmed H3K9me2 loss. Massive retrotransposition does not occur following transposon derepression, but the meiotic chromatin landscape is profoundly affected. Indeed, H3K4me3 marks gained over transcriptionally active transposons correlate with formation of SPO11-dependent double-strand breaks and recruitment of the DMC1 repair enzyme in Dnmt3L(-/-) meiotic cells, whereas these features are normally exclusive to meiotic recombination hot spots. Here, we demonstrate that DNA methylation restrains transposons from adopting chromatin characteristics amenable to meiotic recombination, which we propose prevents the occurrence of erratic chromosomal events.

Indexed as

DNA MethylationAnimalsArgonaute ProteinsChromatinDNA (Cytosine-5-)-MethyltransferasesDNA Transposable ElementsGenomic InstabilityHistonesLong Interspersed Nucleotide ElementsMeiosisMiceMutationRecombination, GeneticSpermatogenesisArgonaute ProteinsChromatinDNA (Cytosine-5-)-MethyltransferasesDNA Transposable ElementsDnmt3l protein, mouseHistonesPIWIL4 protein, mousechromatinDNA methylationfertilitygerm cellsmeiosistransposons

Identifiers

PMID26109049
PMCPMC4495397
OpenAlexW1860278004

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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.