Evidence map›Paper›PMID 10835383›Full record

ArticleGenetics2000

EXO1 and MSH6 are high-copy suppressors of conditional mutations in the MSH2 mismatch repair gene of Saccharomyces cerevisiae.

T Sokolsky, E Alani

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Exonuclease 1 (Exo1) Participates in Mammalian Non-Homologous End Joining and Contributes to Drug Resistance in Ovarian Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2020
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  4. Review
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  9. dNTP pool levels modulate mutator phenotypes of error-prone DNA polymerase ε variants.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  10. Article
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  15. Review
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  18. Antimutator variants of DNA polymerases.Critical reviews in biochemistry and molecular biology · 2011
    Review
  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

2 authors at 1 institution in 1 country.

T SokolskyDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853-2703, USA.
E Alani
Cornell University · US

Funding

Roles for Mismatch Repair Proteins in Maintaining Genome StabilityR01GM053085 · NIGMS · CORNELL UNIVERSITY ITHACA · PI ALANI, ERIC E. · 1995 to 2019
$7.3M
NIGMS NIH HHS R01 GM053085NIGMS NIH HHS R01-GM53085
6 · The paper itself

Abstract

In Saccharomyces cerevisiae, Msh2p, a central component in mismatch repair, forms a heterodimer with Msh3p to repair small insertion/deletion mismatches and with Msh6p to repair base pair mismatches and single-nucleotide insertion/deletion mismatches. In haploids, a msh2Delta mutation is synthetically lethal with pol3-01, a mutation in the Poldelta proofreading exonuclease. Six conditional alleles of msh2 were identified as those that conferred viability in pol3-01 strains at 26 degrees but not at 35 degrees. DNA sequencing revealed that mutations in several of the msh2(ts) alleles are located in regions with previously unidentified functions. The conditional inviability of two mutants, msh2-L560S pol3-01 and msh2-L910P pol3-01, was suppressed by overexpression of EXO1 and MSH6, respectively. Partial suppression was also observed for the temperature-sensitive mutator phenotype exhibited by msh2-L560S and msh2-L910P strains in the lys2-Bgl reversion assay. High-copy plasmids bearing mutations in the conserved EXO1 nuclease domain were unable to suppress msh2-L560S pol3-01 conditional lethality. These results, in combination with a genetic analysis of msh6Delta pol3-01 and msh3Delta pol3-01 strains, suggest that the activity of the Msh2p-Msh6p heterodimer is important for viability in the presence of the pol3-01 mutation and that Exo1p plays a catalytic role in Msh2p-mediated mismatch repair.

Indexed as

Genes, FungalGenes, SuppressorMutationSaccharomyces cerevisiae ProteinsTyrosine 3-Monooxygenase14-3-3 ProteinsAllelesAmino Acid SequenceBase SequenceCatalysisDNA-Binding ProteinsDNA PrimersDNA RepairFungal ProteinsHumansMolecular Sequence Data14-3-3 ProteinsDNA-Binding ProteinsDNA PrimersFungal ProteinsMSH2 protein, S cerevisiaeMSH6 protein, S cerevisiaeMutS Homolog 2 ProteinProteinsSaccharomyces cerevisiae ProteinsTyrosine 3-Monooxygenase

Identifiers

PMID10835383
PMCPMC1461125
OpenAlexW2140132110

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.