Evidence map›Paper›PMID 23599345›Full record

ArticleGenes & development2013

Numerical constraints and feedback control of double-strand breaks in mouse meiosis.

Liisa Kauppi, Marco Barchi, Julian Lange, Frédéric Baudat, Maria Jasin, Scott Keeney

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.

0numbers the graph read from it
0cells of the map it votes in
129citing 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

129 citing papers in PubMed, 192 citations in OpenAlex.

  1. Article
  2. Multifaceted and evolutionarily dynamic interactions betweenbioRxiv : the preprint server for biology · 2026
    Article
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  4. Structure and function of the synaptonemal complex.The Journal of cell biology · 2026
    Review
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  10. Review
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  13. Essential roles of the ANKRD31-REC114 interaction in meiotic recombination and mouse spermatogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Genetic control of meiosis surveillance mechanisms in mammals.Frontiers in cell and developmental biology · 2023
    Review

69 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

6 authors at 4 institutions in 4 countries.

Liisa KauppiMolecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.
Marco Barchi
Julian Lange
Frédéric Baudat
Maria Jasin
Scott Keeney
Memorial Sloan Kettering Cancer Center · USHoward Hughes Medical Institute · USInstitut de Génétique Humaine · FRUniversity of Helsinki · FI

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Role of Spo11 and recombination in mouse meiosisR01HD040916 · NICHD · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI JASIN, MARIA · 2001 to 2011
$5.4M
Role of Spo11 and recombination in mouse meiosisR01GM105421 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI JASIN, MARIA, KEENEY, SCOTT · 2013 to 2016
$2.4M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA008748NICHD NIH HHS R01 HD040916NIGMS NIH HHS R01 GM105421NIGMS NIH HHS R01-GM105421Telethon GGP12189
6 · The paper itself

Abstract

Different organisms display widely different numbers of the programmed double-strand breaks (DSBs) that initiate meiotic recombination (e.g., hundreds per meiocyte in mice and humans vs. dozens in nematodes), but little is known about what drives these species-specific DSB set points or the regulatory pathways that control them. Here we examine male mice with a lowered dosage of SPO11, the meiotic DSB catalyst, to gain insight into the effect of reduced DSB numbers on mammalian chromosome dynamics. An approximately twofold DSB reduction was associated with the reduced ability of homologs to synapse along their lengths, provoking prophase arrest and, ultimately, sterility. In many spermatocytes, chromosome subsets displayed a mix of synaptic failure and synapsis with both homologous and nonhomologous partners ("chromosome tangles"). The X chromosome was nearly always involved in tangles, and small autosomes were involved more often than large ones. We conclude that homolog pairing requirements dictate DSB set points during meiosis. Importantly, our results reveal that karyotype is a key factor: Smaller autosomes and heteromorphic sex chromosomes become weak links when DSBs are reduced below a critical threshold. Unexpectedly, unsynapsed chromosome segments trapped in tangles displayed an elevated density of DSB markers later in meiotic prophase. The unsynapsed portion of the X chromosome in wild-type males also showed evidence that DSB numbers increased as prophase progressed. These findings point to the existence of a feedback mechanism that links DSB number and distribution with interhomolog interactions.

Indexed as

DNA Breaks, Double-StrandedFeedback, PhysiologicalAnimalsChromosomesEndodeoxyribonucleasesMaleMeiosisMeiotic Recombination Protein SPO11MiceSynaptonemal ComplexEndodeoxyribonucleasesMeiotic Recombination Protein SPO11

Identifiers

PMID23599345
PMCPMC3650225
OpenAlexW2138919235

What OpenQuestion holds

Textmetadata
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.