Evidence map›Paper›PMID 28820351›Full record

ArticleCell cycle (Georgetown, Tex.)2017

Genomic and chromatin features shaping meiotic double-strand break formation and repair in mice.

Shintaro Yamada, Seoyoung Kim, Sam E Tischfield, Maria Jasin, Julian Lange, Scott Keeney

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.4field-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

43 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Why recombination hotspots?PLoS genetics · 2026
    Review
  3. Article
  4. Review
  5. Polymorphic transposable elements contribute to variation in recombination landscapes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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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

6 authors at 1 institution in 1 country.

Shintaro Yamadaa Molecular Biology Program, Memorial Sloan Kettering Cancer Center , New York , NY , USA.ORCID http://orcid.org/0000-0002-4882-0871
Seoyoung Kima Molecular Biology Program, Memorial Sloan Kettering Cancer Center , New York , NY , USA.ORCID http://orcid.org/0000-0002-0608-6541
Sam E Tischfielda Molecular Biology Program, Memorial Sloan Kettering Cancer Center , New York , NY , USA.ORCID http://orcid.org/0000-0002-5717-3856
Maria Jasind Developmental Biology Program, Memorial Sloan Kettering Cancer Center , New York , NY , USA.
Julian Langea Molecular Biology Program, Memorial Sloan Kettering Cancer Center , New York , NY , USA.
Scott Keeneya Molecular Biology Program, Memorial Sloan Kettering Cancer Center , New York , NY , USA.ORCID http://orcid.org/0000-0002-1283-6417
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Mechanism and regulation of meiotic recombinationR35GM118092 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI Scott Keeney · 2016 to 2026
$7.0M
Homologous recombination mechanisms in mammalian cellsR35GM118175 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI JASIN, MARIA · 2016 to 2020
$2.6M
Role of Spo11 and recombination in mouse meiosisR01GM105421 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI JASIN, MARIA, KEENEY, SCOTT · 2013 to 2016
$2.4M
NCI NIH HHS P30 CA008748NIGMS NIH HHS R01 GM105421NIGMS NIH HHS R35 GM118092NIGMS NIH HHS R35 GM118175
6 · The paper itself

Abstract

The SPO11-generated DNA double-strand breaks (DSBs) that initiate meiotic recombination occur non-randomly across genomes, but mechanisms shaping their distribution and repair remain incompletely understood. Here, we expand on recent studies of nucleotide-resolution DSB maps in mouse spermatocytes. We find that trimethylation of histone H3 lysine 36 around DSB hotspots is highly correlated, both spatially and quantitatively, with trimethylation of H3 lysine 4, consistent with coordinated formation and action of both PRDM9-dependent histone modifications. In contrast, the DSB-responsive kinase ATM contributes independently of PRDM9 to controlling hotspot activity, and combined action of ATM and PRDM9 can explain nearly two-thirds of the variation in DSB frequency between hotspots. DSBs were modestly underrepresented in most repetitive sequences such as segmental duplications and transposons. Nonetheless, numerous DSBs form within repetitive sequences in each meiosis and some classes of repeats are preferentially targeted. Implications of these findings are discussed for evolution of PRDM9 and its role in hybrid strain sterility in mice. Finally, we document the relationship between mouse strain-specific DNA sequence variants within PRDM9 recognition motifs and attendant differences in recombination outcomes. Our results provide further insights into the complex web of factors that influence meiotic recombination patterns.

Indexed as

DNA Breaks, Double-StrandedGenomeAnimalsAtaxia Telangiectasia Mutated ProteinsBase SequenceBinding SitesCentromereChromatinChromosomes, MammalianCrossing Over, GeneticDNADNA RepairEndodeoxyribonucleasesHistone-Lysine N-MethyltransferaseHistonesMeiosisAtaxia Telangiectasia Mutated ProteinsChromatinDNAEndodeoxyribonucleasesHistone-Lysine N-MethyltransferaseHistonesMeiotic Recombination Protein SPO11prdm9 protein, mousechromatinDNA double-strand breaksmeiosisPRDM9recombinationrepetitive elementsresectionSPO11

Identifiers

PMID28820351
PMCPMC5638367
OpenAlexW2951060263

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.