Evidence map›Paper›PMID 24013428›Full record

ArticleCell cycle (Georgetown, Tex.)2013

Clamping down on mammalian meiosis.

Amy M Lyndaker, Ana Vasileva, Debra J Wolgemuth, Robert S Weiss, Howard B Lieberman

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Whole genome sequencing identifies allelic ratio distortion in sperm involving genes related to spermatogenesis in a swine model.DNA research : an international journal for rapid publication of reports on genes and genomes · 2020
    Article
  8. Review
  9. Article
  10. The meiotic checkpoint network: step-by-step through meiotic prophase.Cold Spring Harbor perspectives in biology · 2014
    Review
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

5 authors at 5 institutions in 4 countries.

Amy M LyndakerDepartment of Biomedical Sciences; Cornell University; Ithaca, NY USA
Ana VasilevaCenter for Radiological Research; College of Physicians and Surgeons; Columbia University Medical Center; New York, NY USA
Debra J WolgemuthGenetics & Development and Obstetrics & Gynecology; The Institute of Human Nutrition; Herbert Irving Comprehensive Cancer Center; Columbia University Medical Center; New York, NY USA
Robert S WeissDepartment of Biomedical Sciences; Cornell University; Ithaca, NY USA
Howard B LiebermanDepartment of Environmental Health Sciences; Mailman School of Public Health; Columbia University Medical Center; New York, NY USA.
Columbia University Irving Medical Center · USCornell University · USIthaca College · USNew York Proton Center · USRoyal College of Physicians · GB

Funding

The MRAD9 Radioresistance GeneR01GM079107 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LIEBERMAN, HOWARD B. · 2006 to 2013
$2.6M
Genome maintenance by the mouse Hus1 checkpoint geneR01CA108773 · NCI · CORNELL UNIVERSITY ITHACA · PI WEISS, ROBERT S · 2004 to 2013
$2.5M
Reproductive Sciences and Genomics Training ProgramT32HD052471 · NICHD · CORNELL UNIVERSITY · PI ROBERSON, MARK S · 2007 to 2016
$2.0M
NCI NIH HHS R01 CA108773NICHD NIH HHS T32 HD052471NIGMS NIH HHS GM079107NIGMS NIH HHS R01 GM079107
6 · The paper itself

Abstract

The RAD9A-RAD1-HUS1 (9-1-1) complex is a PCNA-like heterotrimeric clamp that binds damaged DNA to promote cell cycle checkpoint signaling and DNA repair. While various 9-1-1 functions in mammalian somatic cells have been established, mounting evidence from lower eukaryotes predicts critical roles in meiotic germ cells as well. This was investigated in 2 recent studies in which the 9-1-1 complex was disrupted specifically in the mouse male germline through conditional deletion of Rad9a or Hus1. Loss of these clamp subunits led to severely impaired fertility and meiotic defects, including faulty DNA double-strand break repair. While 9-1-1 is critical for ATR kinase activation in somatic cells, these studies did not reveal major defects in ATR checkpoint pathway signaling in meiotic cells. Intriguingly, this new work identified separable roles for 9-1-1 subunits, namely RAD9A- and HUS1-independent roles for RAD1. Based on these studies and the high-level expression of the paralogous proteins RAD9B and HUS1B in testis, we propose a model in which multiple alternative 9-1-1 clamps function during mammalian meiosis to ensure genome maintenance in the germline.

Indexed as

MeiosisAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA RepairExonucleasesFertilityGerm CellsMaleMiceRecombination, GeneticSignal TransductionAtaxia Telangiectasia Mutated ProteinsAtr protein, mouseCell Cycle ProteinsExonucleasesHus1 protein, mouseRad1 protein, mouserad9 proteinATRdouble-strand break repairHUS1Bmeiosispachytene checkpointRAD9A-RAD1-HUS1 complexRAD9BsynapsisTOPBP1

Identifiers

PMID24013428
PMCPMC3865008
OpenAlexW1971278776

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.