Evidence map›Paper›PMID 35133274›Full record

ArticleeLife2022

Multiple 9-1-1 complexes promote homolog synapsis, DSB repair, and ATR signaling during mammalian meiosis.

Catalina Pereira, Gerardo A Arroyo-Martinez, Matthew Z Guo, Michael S Downey, Emma R Kelly, Kathryn J Grive, Shantha K Mahadevaiah, Jennie R Sims, Vitor M Faca, Charlton Tsai and 11 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

4 citing papers in PubMed, 12 citations in OpenAlex.

  1. The 9-1-1 complex protects ssDNA gaps in BRCA2-deficient cancer.bioRxiv : the preprint server for biology · 2025
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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

21 authors at 9 institutions in 5 countries.

Catalina PereiraDepartment of Biomedical Sciences, Cornell University, Ithaca, United States.ORCID 0000-0003-3144-0909
Gerardo A Arroyo-MartinezDepartment of Biomedical Sciences, Cornell University, Ithaca, United States.ORCID 0000-0003-2308-3286
Matthew Z GuoDepartment of Biomedical Sciences, Cornell University, Ithaca, United States.ORCID 0000-0003-4741-7463
Michael S DowneyDepartment of Biomedical Sciences, Cornell University, Ithaca, United States.ORCID 0000-0001-9818-5274
Emma R KellyDivision of Mathematics and Natural Sciences, Elmira College, Elmira, United States.
Kathryn J GriveDepartment of Obstetrics and Gynecology, Brown University, Providence, United States.
Shantha K MahadevaiahSex Chromosome Biology Laboratory, The Francis Crick Institute, London, United Kingdom.
Jennie R SimsDepartment of Molecular Biology and Genetics, Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, United States.
Vitor M FacaDepartment of Biochemistry and Immunology, FMRP, University of São Paulo, Ribeirão Preto, Brazil.
Charlton TsaiDepartment of Biomedical Sciences, Cornell University, Ithaca, United States.
Carl J SchiltzDepartment of Biomedical Sciences, Cornell University, Ithaca, United States.
Niek WitDivision of Immunology, The Netherlands Cancer Institute, Amsterdam, Netherlands.
Heinz JacobsDivision of Immunology, The Netherlands Cancer Institute, Amsterdam, Netherlands.
Nathan L ClarkDepartment of Human Genetics, University of Utah, Salt Lake City, United States.ORCID 0000-0003-0006-8374
Raimundo FreireUnidad de Investigación, Hospital Universitario de Canarias, Tenerife, Spain.ORCID 0000-0003-4473-8894
James TurnerSex Chromosome Biology Laboratory, The Francis Crick Institute, London, United Kingdom.ORCID 0000-0003-1722-7677
Amy M LyndakerDivision of Mathematics and Natural Sciences, Elmira College, Elmira, United States.
Miguel A Brieno-EnriquezMagee-Womens Research Institute, Department of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, United States.
Paula E CohenDepartment of Biomedical Sciences, Cornell University, Ithaca, United States.ORCID 0000-0002-2050-6979
Marcus B SmolkaDepartment of Molecular Biology and Genetics, Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, United States.ORCID 0000-0001-9952-2885
Robert S WeissDepartment of Biomedical Sciences, Cornell University, Ithaca, United States.ORCID 0000-0003-3327-1379
Cornell University · USElmira College · USThe Francis Crick Institute · GBThe Netherlands Cancer Institute · NLJohn Brown University · USUniversidad de La Laguna · ESUniversidade de São Paulo · BRUniversity of Pittsburgh · USUniversity of Utah · US

Funding

The MLH1-MLH3 Heterodimer in Mammalian Meiotic Recombination and GameogenesisR01HD041012 · NICHD · YESHIVA UNIVERSITY · PI Paula Elaine Cohen · 2003 to 2026
$7.9M
UNIVERSITY OF PUERTO RICO PONCE RESEARCH INITIATIVE FOR SCIENTIFIC ENHANCEMENT: UR25GM096955 · NIGMS · UNIVERSITY OF PUERTO RICO PONCE · PI SUAREZ-MARTINEZ, EDU B · 2011 to 2020
$5.7M
Coordination of ATR Signaling for Genetic Quality Control, Silencing, and DNA Repair During MeiosisR01HD095296 · NICHD · CORNELL UNIVERSITY · PI Paula Elaine Cohen, Marcus Smolka · 2018 to 2026
$4.2M
Discovery and characterization of ocular regulatory elements through evolutionary analysisR01EY030546 · NEI · UNIVERSITY OF UTAH · PI CHIKINA, MARIA D, CLARK, NATHANIEL L · 2020 to 2024
$2.4M
SLX4 as a mediator of crossover pathway decisions in mammalian meiosisR01HD097987 · NICHD · CORNELL UNIVERSITY · PI COHEN, PAULA ELAINE · 2019 to 2023
$1.9M
Mark I Model 68 Gamma IrradiatorS10RR023781 · NCRR · CORNELL UNIVERSITY · PI WEISS, ROBERT S · 2007 to 2007
$234k
Germline Roles for the RAD1 Checkpoint Protein in Genomic Integrity and FertilityR03HD083621 · NICHD · CORNELL UNIVERSITY · PI WEISS, ROBERT S · 2016 to 2017
$155k
Cancer Research UK FC001193Medical Research Council FC001193NCRR NIH HHS S10 RR023781NEI NIH HHS R01 EY030546NICHD NIH HHS R01 HD041012NICHD NIH HHS R01 HD095296NICHD NIH HHS R01 HD097987NICHD NIH HHS R03 HD083621NIGMS NIH HHS R25 GM096955Wellcome Trust FC001193
6 · The paper itself

Abstract

DNA damage response mechanisms have meiotic roles that ensure successful gamete formation. While completion of meiotic double-strand break (DSB) repair requires the canonical RAD9A-RAD1-HUS1 (9A-1-1) complex, mammalian meiocytes also express RAD9A and HUS1 paralogs, RAD9B and HUS1B, predicted to form alternative 9-1-1 complexes. The RAD1 subunit is shared by all predicted 9-1-1 complexes and localizes to meiotic chromosomes even in the absence of HUS1 and RAD9A. Here, we report that testis-specific disruption of RAD1 in mice resulted in impaired DSB repair, germ cell depletion, and infertility. Unlike

Indexed as

Chromosome PairingDNA RepairMeiosisAnimalsAtaxia Telangiectasia Mutated ProteinsDNA-Binding ProteinsDNA Breaks, Double-StrandedMaleMiceMice, TransgenicSignal TransductionTestisAtaxia Telangiectasia Mutated ProteinsDNA-Binding Proteins9-1-1 complexATRcell biologyDNA break repairDNA damage responsegeneticsgenomicsmeiosismeiotic silencingmouse

Identifiers

PMID35133274
PMCPMC8824475
OpenAlexW4225433532

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.