Evidence map›Paper›PMID 28617799›Full record

ArticlePLoS genetics2017

p53 and TAp63 participate in the recombination-dependent pachytene arrest in mouse spermatocytes.

Marina Marcet-Ortega, Sarai Pacheco, Ana Martínez-Marchal, Helena Castillo, Elsa Flores, Maria Jasin, Scott Keeney, Ignasi Roig

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.9field-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

38 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. GWAS-Identified SNPs and Candidate Genes Influencing Sex in Loach (Animals : an open access journal from MDPI · 2026
    Article
  6. Article
  7. Mouse X-linked microRNA cluster regulates the meiotic checkpoint andProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Genetic control of meiosis surveillance mechanisms in mammals.Frontiers in cell and developmental biology · 2023
    Review
  16. p53 Controls Meiotic Prophase Progression and Crossover Formation.International journal of molecular sciences · 2022
    Article
  17. Article
  18. eLife · 2022
    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

8 authors at 3 institutions in 2 countries.

Marina Marcet-OrtegaGenome Integrity and Instability Group, Institut de Biotecnologia i Biomedicina, Universitat Autònoma de Barcelona, Cerdanyola del Vallès, Barcelona, Spain.ORCID http://orcid.org/0000-0002-5756-1373
Sarai PachecoGenome Integrity and Instability Group, Institut de Biotecnologia i Biomedicina, Universitat Autònoma de Barcelona, Cerdanyola del Vallès, Barcelona, Spain.ORCID http://orcid.org/0000-0002-3425-4901
Ana Martínez-MarchalGenome Integrity and Instability Group, Institut de Biotecnologia i Biomedicina, Universitat Autònoma de Barcelona, Cerdanyola del Vallès, Barcelona, Spain.
Helena CastilloGenome Integrity and Instability Group, Institut de Biotecnologia i Biomedicina, Universitat Autònoma de Barcelona, Cerdanyola del Vallès, Barcelona, Spain.
Elsa FloresDepartment of Biochemistry and Molecular Biology, Graduate School of Biomedical Sciences, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, United States of America.
Maria JasinDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America.
Scott KeeneyMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America.ORCID http://orcid.org/0000-0002-1283-6417
Ignasi RoigGenome Integrity and Instability Group, Institut de Biotecnologia i Biomedicina, Universitat Autònoma de Barcelona, Cerdanyola del Vallès, Barcelona, Spain.ORCID http://orcid.org/0000-0003-0313-3581
Universitat Autònoma de Barcelona · ESMemorial Sloan Kettering Cancer Center · USThe University of Texas MD Anderson 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

To protect germ cells from genomic instability, surveillance mechanisms ensure meiosis occurs properly. In mammals, spermatocytes that display recombination defects experience a so-called recombination-dependent arrest at the pachytene stage, which relies on the MRE11 complex-ATM-CHK2 pathway responding to unrepaired DNA double-strand breaks (DSBs). Here, we asked if p53 family members-targets of ATM and CHK2-participate in this arrest. We bred double-mutant mice combining a mutation of a member of the p53 family (p53, TAp63, or p73) with a Trip13 mutation. Trip13 deficiency triggers a recombination-dependent response that arrests spermatocytes in pachynema before they have incorporated the testis-specific histone variant H1t into their chromatin. We find that deficiency for either p53 or TAp63, but not p73, allowed spermatocytes to progress further into meiotic prophase despite the presence of numerous unrepaired DSBs. Even so, the double mutant spermatocytes apoptosed at late pachynema because of sex body deficiency; thus p53 and TAp63 are dispensable for arrest caused by sex body defects. These data affirm that recombination-dependent and sex body-deficient arrests occur via genetically separable mechanisms.

Indexed as

Recombination, GeneticAnimalsApoptosisCell Cycle CheckpointsChromatinDNA Breaks, Double-StrandedDNA RepairHistonesMaleMeiosisMicePachytene StagePhosphoproteinsSpermatocytesTestisTrans-ActivatorsChromatinHistonesPhosphoproteinsTrans-ActivatorsTrp63 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID28617799
PMCPMC5491309
OpenAlexW2625409803

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.