Evidence map›Paper›PMID 30944090›Full record

ArticleG3 (Bethesda, Md.)2019

Mutation of the ATPase Domain of MutS Homolog-5 (MSH5) Reveals a Requirement for a Functional MutSγ Complex for All Crossovers in Mammalian Meiosis.

Carolyn R Milano, J Kim Holloway, Yongwei Zhang, Bo Jin, Cameron Smith, Aviv Bergman, Winfried Edelmann, Paula E Cohen

Open access · goldAbstract read
In one paragraph

Article in G3 (Bethesda, Md.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 25% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  15. Cell genomics · 2023
    Article
  16. Article
  17. A Homozygous Loss-of-Function Mutation inInternational journal of molecular sciences · 2022
    Article
  18. Robust designation of meiotic crossover sites by CDK-2 through phosphorylation of the MutSγ complex.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  19. Plant physiology · 2020
    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 2 institutions in 1 country.

Carolyn R MilanoDepartment of Biomedical Sciences and Center for Reproductive Genomics, Cornell University, Ithaca, NY 14853.ORCID 0000-0003-1261-3763
J Kim HollowayDepartment of Biomedical Sciences and Center for Reproductive Genomics, Cornell University, Ithaca, NY 14853.
Yongwei ZhangDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461.
Bo JinDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461.
Cameron SmithDepartment of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY 10461.
Aviv BergmanDepartment of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY 10461.
Winfried EdelmannDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461 paula.cohen@cornell.edu winfried.edelmann@einstein.yu.edu.
Paula E CohenDepartment of Biomedical Sciences and Center for Reproductive Genomics, Cornell University, Ithaca, NY 14853 paula.cohen@cornell.edu winfried.edelmann@einstein.yu.edu.ORCID 0000-0002-2050-6979
Albert Einstein College of Medicine · USCornell University · US

Funding

The MLH1-MLH3 Heterodimer in Mammalian Meiotic Recombination and GameogenesisR01HD041012 · NICHD · YESHIVA UNIVERSITY · PI Paula Elaine Cohen · 2003 to 2026
$7.9M
DNA MISMATCH REPAIR AND CANCER IN MURINE MODELSR01CA076329 · NCI · YESHIVA UNIVERSITY · PI EDELMANN, WINFRIED · 1998 to 2017
$6.9M
Genetic Pathways Effecting Crossover Control and Meiotic Recombination in MammalsR01GM097263 · NIGMS · CORNELL UNIVERSITY · PI COHEN, PAULA ELAINE · 2012 to 2015
$1.1M
NCI NIH HHS R01 CA076329NICHD NIH HHS R01 HD041012NIGMS NIH HHS R01 GM097263
6 · The paper itself

Abstract

During meiosis, induction of DNA double strand breaks (DSB) leads to recombination between homologous chromosomes, resulting in crossovers (CO) and non-crossovers (NCO). In the mouse, only 10% of DSBs resolve as COs, mostly through a class I pathway dependent on MutSγ (MSH4/ MSH5) and MutLγ (MLH1/MLH3), the latter representing the ultimate marker of these CO events. A second Class II CO pathway accounts for only a few COs, but is not thought to involve MutSγ/ MutLγ, and is instead dependent on MUS81-EME1. For class I events, loading of MutLγ is thought to be dependent on MutSγ, however MutSγ loads very early in prophase I at a frequency that far exceeds the final number of class I COs. Moreover, loss of MutSγ in mouse results in apoptosis before CO formation, preventing the analysis of its CO function. We generated a mutation in the ATP binding domain of

Indexed as

MutationAdenosine TriphosphatasesAdenosine TriphosphateAnimalsCell Cycle ProteinsDNA-Binding ProteinsMaleMammalsMeiosisMiceMice, KnockoutMultiprotein ComplexesPhenotypeProtein BindingProtein DomainsProtein Interaction Domains and MotifsAdenosine TriphosphatasesAdenosine TriphosphateCell Cycle ProteinsDNA-Binding ProteinsMsh5 protein, mouseMultiprotein Complexescrossing overcrossover designationhomologous recombinationmeiosismouseMutS homologprophase I

Identifiers

PMID30944090
PMCPMC6553527
OpenAlexW2915049380

What OpenQuestion holds

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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.