Evidence map›Paper›PMID 12529393›Full record

ArticleMolecular and cellular biology2003

Systematic mutagenesis of the Saccharomyces cerevisiae MLH1 gene reveals distinct roles for Mlh1p in meiotic crossing over and in vegetative and meiotic mismatch repair.

Juan Lucas Argueso, Amanda Wraith Kijas, Sumeet Sarin, Julie Heck, Marc Waase, Eric Alani

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Insights into DNA cleavage by MutL homologs from analysis of conserved motifs in eukaryotic Mlh1.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023
    Article
  7. Article
  8. Article
  9. Enforcement of Postzygotic Species Boundaries in the Fungal Kingdom.Microbiology and molecular biology reviews : MMBR · 2022
    Review
  10. The unstructured linker of Mlh1 contains a motif required for endonuclease function which is mutated in cancers.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  11. Review
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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

6 authors at 1 institution in 1 country.

Juan Lucas ArguesoDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853-2703, USA.
Amanda Wraith Kijas
Sumeet Sarin
Julie Heck
Marc Waase
Eric 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 GM53085NIGMS NIH HHS R01 GM053085
6 · The paper itself

Abstract

In eukaryotic cells, DNA mismatch repair is initiated by a conserved family of MutS (Msh) and MutL (Mlh) homolog proteins. Mlh1 is unique among Mlh proteins because it is required in mismatch repair and for wild-type levels of crossing over during meiosis. In this study, 60 new alleles of MLH1 were examined for defects in vegetative and meiotic mismatch repair as well as in meiotic crossing over. Four alleles predicted to disrupt the Mlh1p ATPase activity conferred defects in all functions assayed. Three mutations, mlh1-2, -29, and -31, caused defects in mismatch repair during vegetative growth but allowed nearly wild-type levels of meiotic crossing over and spore viability. Surprisingly, these mutants did not accumulate high levels of postmeiotic segregation at the ARG4 recombination hotspot. In biochemical assays, Pms1p failed to copurify with mlh1-2, and two-hybrid studies indicated that this allele did not interact with Pms1p and Mlh3p but maintained wild-type interactions with Exo1p and Sgs1p. mlh1-29 and mlh1-31 did not alter the ability of Mlh1p-Pms1p to form a ternary complex with a mismatch substrate and Msh2p-Msh6p, suggesting that the region mutated in these alleles could be responsible for signaling events that take place after ternary complex formation. These results indicate that mismatches formed during genetic recombination are processed differently than during replication and that, compared to mismatch repair functions, the meiotic crossing-over role of MLH1 appears to be more resistant to mutagenesis, perhaps indicating a structural role for Mlh1p during crossing over.

Indexed as

Genes, FungalAdaptor Proteins, Signal TransducingAdenosine TriphosphatasesAdenosine TriphosphateAllelesBase Pair MismatchCarrier ProteinsCrossing Over, GeneticDNA RepairFungal ProteinsMeiosisMutagenesisMutL Protein Homolog 1MutL ProteinsPhenotypeProtein Structure, TertiaryAdaptor Proteins, Signal TransducingAdenosine TriphosphatasesAdenosine TriphosphateCarrier ProteinsFungal ProteinsMLH1 protein, S cerevisiaeMutL Protein Homolog 1MutL ProteinsPMS1 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID12529393
PMCPMC140715
OpenAlexW2153436066

What OpenQuestion holds

Textmetadata
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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.