Evidence map›Paper›PMID 26440409›Full record

ArticleChromosoma2016

A surge of late-occurring meiotic double-strand breaks rescues synapsis abnormalities in spermatocytes of mice with hypomorphic expression of SPO11.

Monica Faieta, Stefano Di Cecca, Dirk G de Rooij, Andrea Luchetti, Michela Murdocca, Monica Di Giacomo, Sara Di Siena, Manuela Pellegrini, Pellegrino Rossi, Marco Barchi

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Chromosoma, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

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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

10 authors at 5 institutions in 2 countries.

Monica FaietaDepartment of Biomedicine and Prevention, Section of Anatomy, University of Rome Tor Vergata, 00133, Rome, Italy.
Stefano Di CeccaDepartment of Biomedicine and Prevention, Section of Anatomy, University of Rome Tor Vergata, 00133, Rome, Italy.
Dirk G de RooijReproductive Biology Group, Division of Developmental Biology, Department of Biology, Faculty of Science, Utrecht University, Utrecht, Netherlands.
Andrea LuchettiDepartment of Biomedicine and Prevention, Section of Genetics, University of Rome Tor Vergata, 00133, Rome, Italy.
Michela MurdoccaDepartment of Biomedicine and Prevention, Section of Genetics, University of Rome Tor Vergata, 00133, Rome, Italy.
Monica Di GiacomoEuropean Molecular Biology Laboratory (EMBL), Monterotondo, Italy.
Sara Di SienaDAHFMO, Sapienza University, Rome, Italy.
Manuela PellegriniDepartment of Medicine and Health Science "Vincenzo Tiberio", University of Molise, Campobasso, Italy.
Pellegrino RossiDepartment of Biomedicine and Prevention, Section of Anatomy, University of Rome Tor Vergata, 00133, Rome, Italy.
Marco BarchiDepartment of Biomedicine and Prevention, Section of Anatomy, University of Rome Tor Vergata, 00133, Rome, Italy. marco.barchi@uniroma2.it.
University of Rome Tor Vergata · ITEuropean Molecular Biology Laboratory · ITSapienza University of Rome · ITUniversity of Amsterdam · NLUniversity of Molise · IT

Funding

Telethon GGP12189
6 · The paper itself

Abstract

Meiosis is the biological process that, after a cycle of DNA replication, halves the cellular chromosome complement, leading to the formation of haploid gametes. Haploidization is achieved via two successive rounds of chromosome segregation, meiosis I and II. In mammals, during prophase of meiosis I, homologous chromosomes align and synapse through a recombination-mediated mechanism initiated by the introduction of DNA double-strand breaks (DSBs) by the SPO11 protein. In male mice, if SPO11 expression and DSB number are reduced below heterozygosity levels, chromosome synapsis is delayed, chromosome tangles form at pachynema, and defective cells are eliminated by apoptosis at epithelial stage IV at a spermatogenesis-specific endpoint. Whether DSB levels produced in Spo11 (+/-) spermatocytes represent, or approximate, the threshold level required to guarantee successful homologous chromosome pairing is unknown. Using a mouse model that expresses Spo11 from a bacterial artificial chromosome, within a Spo11 (-/-) background, we demonstrate that when SPO11 expression is reduced and DSBs at zygonema are decreased (approximately 40 % below wild-type level), meiotic chromosome pairing is normal. Conversely, DMC1 foci number is increased at pachynema, suggesting that under these experimental conditions, DSBs are likely made with delayed kinetics at zygonema. In addition, we provide evidences that when zygotene-like cells receive enough DSBs before chromosome tangles develop, chromosome synapsis can be completed in most cells, preventing their apoptotic elimination.

Indexed as

Chromosome PairingDNA Breaks, Double-StrandedMeiosisAnimalsChromosomesEndodeoxyribonucleasesFemaleMaleMeiotic Prophase IMeiotic Recombination Protein SPO11MiceMice, Inbred C57BLMice, KnockoutSpermatocytesSpermatogenesisEndodeoxyribonucleasesMeiotic Recombination Protein SPO11Chromosome synapsisDouble-strand breaks (DSBs)MeiosisMeiotic recombinationSpermatogenesisSPO11

Identifiers

PMID26440409
PMCPMC4830894
OpenAlexW1902427536

What OpenQuestion holds

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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.