Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Negative epistasis between natural variants of the Saccharomyces cerevisiae MLH1 and PMS1 genes results in a defect in mismatch repair.

Proceedings of the National Academy of Sciences of the United States of America - 28 Feb 2006

Heck Julie Akiko, Argueso Juan Lucas, Gemici Zekeriyya, Reeves Richard Guy, Bernard Ann, Aquadro Charles F, Alani Eric

Abstract excerpt

In budding yeast, the MLH1-PMS1 heterodimer is the major MutL homolog complex that acts to repair mismatches arising during DNA replication. Using a highly sensitive mutator assay, we observed that Saccharomyces cerevisiae strains bearing the S288c-strain-derived MLH1 gene and the SK1-strain-derived PMS1 gene displayed elevated mutation rates that conferred a long-term fitness cost. Dissection of this negative...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adaptor Proteins, Signal Transducing
Share to Base Pair Mismatch

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to DNA, Fungal

Share to DNA, Recombinant

Share to Epistasis, Genetic

Share to Fungal Proteins

Share to MutL Protein Homolog 1

Share to MutL Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 16492773
DOI: 10.1073/pnas.0510998103
PMCID: PMC1413905

Genes

MLH1
PMS1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Negative epistasis between natural variants of the Saccharomyces cerevisiae MLH1 and PMS1 genes results in a defect in mismatch repair.PMID 16492773Read ↗

Mismatch Repair Incompatibilities in Diverse Yeast Populations.Semantic proximity Read ↗

Incompatibilities involving yeast mismatch repair genes: a role for genetic modifiers and implications for disease penetrance and variation in genomic mutation rates.Semantic proximity Read ↗

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

Analysis of conditional mutations in the Saccharomyces cerevisiae MLH1 gene in mismatch repair and in meiotic crossing over.Semantic proximity Read ↗

Mutation rates, spectra, and genome-wide distribution of spontaneous mutations in mismatch repair deficient yeast.Semantic proximity Read ↗

Functional specificity of MutL homologs in yeast: evidence for three Mlh1-based heterocomplexes with distinct roles during meiosis in recombination and mismatch correction.Semantic proximity Read ↗

Mlh1 is unique among mismatch repair proteins in its ability to promote crossing-over during meiosis.Semantic proximity Read ↗

The effect of genetic background on the function of Saccharomyces cerevisiae mlh1 alleles that correspond to HNPCC missense mutations.Semantic proximity Read ↗

Mutator phenotype due to loss of heterozygosity in diploid yeast strains with mutations in MSH2 and MLH1.Semantic proximity Read ↗

Mutator phenotypes conferred by MLH1 overexpression and by heterozygosity for mlh1 mutations.Semantic proximity Read ↗

Signification and Application of Mutator and Antimutator Phenotype-Induced Genetic Variations in Evolutionary Adaptation and Cancer Therapeutics.Semantic proximity Read ↗

Dual requirement in yeast DNA mismatch repair for MLH1 and PMS1, two homologs of the bacterial mutL gene.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.