Evidence map›Paper›PMID 27745971›Full record

ArticleCell2016

The Landscape of Mouse Meiotic Double-Strand Break Formation, Processing, and Repair.

Julian Lange, Shintaro Yamada, Sam E Tischfield, Jing Pan, Seoyoung Kim, Xuan Zhu, Nicholas D Socci, Maria Jasin, Scott Keeney

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed
20.0field-weighted citation impact, top 1% 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

196 citing papers in PubMed, 315 citations in OpenAlex.

  1. Controlling Meiotic Double-Strand Break Formation in Mice: A Web of Multivalent Protein-Protein Interactions.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  2. Article
  3. Article
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  10. Why recombination hotspots?PLoS genetics · 2026
    Review
  11. High-resolution global recombination mapping inbioRxiv : the preprint server for biology · 2026
    Article
  12. Article
  13. Article
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  15. Article
  16. Ufd2p promotes efficient crossover formation by destabilizing Top2p during meiosis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  17. Article
  18. Article
  19. Article
  20. Article

136 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

9 authors at 4 institutions in 1 country.

Julian LangeMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Shintaro YamadaMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Memorial Sloan Kettering Cancer Center, Howard Hughes Medical Institute, New York, NY 10065, USA.
Sam E TischfieldMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Tri-Institutional Training Program in Computational Biology and Medicine, Weill Cornell Medical College, New York, NY 10065, USA.
Jing PanMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Seoyoung KimMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Xuan ZhuMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Weill Cornell Graduate School of Medical Sciences, New York, NY 10065, USA.
Nicholas D SocciBioinformatics Core, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Maria JasinWeill Cornell Graduate School of Medical Sciences, New York, NY 10065, USA; Developmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Electronic address: m-jasin@ski.mskcc.org.
Scott KeeneyMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Memorial Sloan Kettering Cancer Center, Howard Hughes Medical Institute, New York, NY 10065, USA; Weill Cornell Graduate School of Medical Sciences, New York, NY 10065, USA. Electronic address: s-keeney@ski.mskcc.org.
Memorial Sloan Kettering Cancer Center · USCornell University · USHoward Hughes Medical Institute · USTri-Institutional PhD Program in Chemical Biology · 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
Mechanism of meiotic recombination in yeastR01GM058673 · NIGMS · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI KEENEY, SCOTT · 1999 to 2015
$6.0M
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
Mechanism and distribution of meiotic recombination initiation in mouseR01HD053855 · NICHD · SLOAN-KETTERING INST CAN RESEARCH · PI JASIN, MARIA, KEENEY, SCOTT · 2009 to 2013
$1.9M
NCI NIH HHS P30 CA008748NICHD NIH HHS R01 HD053855NIGMS NIH HHS R01 GM058673NIGMS NIH HHS R01 GM105421NIGMS NIH HHS R35 GM118092NIGMS NIH HHS R35 GM118175
6 · The paper itself

Abstract

Heritability and genome stability are shaped by meiotic recombination, which is initiated via hundreds of DNA double-strand breaks (DSBs). The distribution of DSBs throughout the genome is not random, but mechanisms molding this landscape remain poorly understood. Here, we exploit genome-wide maps of mouse DSBs at unprecedented nucleotide resolution to uncover previously invisible spatial features of recombination. At fine scale, we reveal a stereotyped hotspot structure-DSBs occur within narrow zones between methylated nucleosomes-and identify relationships between SPO11, chromatin, and the histone methyltransferase PRDM9. At large scale, DSB formation is suppressed on non-homologous portions of the sex chromosomes via the DSB-responsive kinase ATM, which also shapes the autosomal DSB landscape at multiple size scales. We also provide a genome-wide analysis of exonucleolytic DSB resection lengths and elucidate spatial relationships between DSBs and recombination products. Our results paint a comprehensive picture of features governing successive steps in mammalian meiotic recombination.

Indexed as

DNA Breaks, Double-StrandedDNA RepairHomologous RecombinationAnimalsAtaxia Telangiectasia Mutated ProteinsChromatinDNA MethylationEndodeoxyribonucleasesGenomic InstabilityHistone-Lysine N-MethyltransferaseMeiosisMeiotic Recombination Protein SPO11MiceMice, Inbred C57BLNucleosomesX ChromosomeAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseChromatinEndodeoxyribonucleasesHistone-Lysine N-MethyltransferaseMeiotic Recombination Protein SPO11Nucleosomesprdm9 protein, mousechromatinDNA damageDNA repairdouble-strand breakhomologous recombinationmeiosismousePRDM9resectionSPO11

Identifiers

PMID27745971
PMCPMC5117687
OpenAlexW2531301510

What OpenQuestion holds

Textmetadata
LicenceTDM
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.