Evidence map›Paper›PMID 30393076›Full record

ArticleDevelopmental cell2018

SETDB1 Links the Meiotic DNA Damage Response to Sex Chromosome Silencing in Mice.

Takayuki Hirota, Paul Blakeley, Mahesh N Sangrithi, Shantha K Mahadevaiah, Vesela Encheva, Ambrosius P Snijders, Elias ElInati, Obah A Ojarikre, Dirk G de Rooij, Kathy K Niakan and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Developmental cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.0field-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

56 citing papers in PubMed, 104 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The Many Faces of SetDB1.Epigenomes · 2026
    Review
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  7. Article
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  18. Kdm4d mutant mice show impaired sperm motility and subfertility.The Journal of reproduction and development · 2024
    Article
  19. Article
  20. Article
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

11 authors at 3 institutions in 3 countries.

Takayuki HirotaSex Chromosome Biology Laboratory, The Francis Crick Institute, London NW1 1AT, UK.
Paul BlakeleyHuman Embryo and Stem Cell Laboratory, The Francis Crick Institute, London NW1 1AT, UK.
Mahesh N SangrithiKK Women's and Children's Hospital, Department of Reproductive Medicine, Singapore 229899, Singapore; Duke-NUS Graduate Medical School, Singapore 119077, Singapore.
Shantha K MahadevaiahSex Chromosome Biology Laboratory, The Francis Crick Institute, London NW1 1AT, UK.
Vesela EnchevaMass Spectrometry Science Technology Platform, The Francis Crick Institute, London NW1 1AT, UK.
Ambrosius P SnijdersMass Spectrometry Science Technology Platform, The Francis Crick Institute, London NW1 1AT, UK.
Elias ElInatiSex Chromosome Biology Laboratory, The Francis Crick Institute, London NW1 1AT, UK.
Obah A OjarikreSex Chromosome Biology Laboratory, The Francis Crick Institute, London NW1 1AT, UK.
Dirk G de RooijReproductive Biology Group, Division of Developmental Biology, Department of Biology, Faculty of Science, Utrecht University, Utrecht 3584 CH, the Netherlands; Center for Reproductive Medicine, Academic Medical Center, University of Amsterdam, Amsterdam 1105 AZ, the Netherlands.
Kathy K NiakanHuman Embryo and Stem Cell Laboratory, The Francis Crick Institute, London NW1 1AT, UK.
James M A TurnerSex Chromosome Biology Laboratory, The Francis Crick Institute, London NW1 1AT, UK. Electronic address: james.turner@crick.ac.uk.
The Francis Crick Institute · GBKK Women's and Children's Hospital · SGUtrecht University · NL

Funding

Medical Research Council FC001120Medical Research Council FC001193Wellcome Trust FC001120Wellcome Trust FC001193
6 · The paper itself

Abstract

Meiotic synapsis and recombination ensure correct homologous segregation and genetic diversity. Asynapsed homologs are transcriptionally inactivated by meiotic silencing, which serves a surveillance function and in males drives meiotic sex chromosome inactivation. Silencing depends on the DNA damage response (DDR) network, but how DDR proteins engage repressive chromatin marks is unknown. We identify the histone H3-lysine-9 methyltransferase SETDB1 as the bridge linking the DDR to silencing in male mice. At the onset of silencing, X chromosome H3K9 trimethylation (H3K9me3) enrichment is downstream of DDR factors. Without Setdb1, the X chromosome accrues DDR proteins but not H3K9me3. Consequently, sex chromosome remodeling and silencing fail, causing germ cell apoptosis. Our data implicate TRIM28 in linking the DDR to SETDB1 and uncover additional factors with putative meiotic XY-silencing functions. Furthermore, we show that SETDB1 imposes timely expression of meiotic and post-meiotic genes. Setdb1 thus unites the DDR network, asynapsis, and meiotic chromosome silencing.

Indexed as

Chromosome PairingDNA DamageGene SilencingHistone CodeAnimalsApoptosisDNA RepairHistone-Lysine N-MethyltransferaseHistonesMaleMiceMice, Inbred C57BLTripartite Motif-Containing Protein 28Histone-Lysine N-MethyltransferaseHistonesSETDB1 protein, mouseTrim28 protein, mouseTripartite Motif-Containing Protein 28DNA damage responseH3K9me3meiotic silencingmouseMSCIsex chromosomes

Identifiers

PMID30393076
PMCPMC6286383
OpenAlexW2899394207

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.