ArticleNucleic acids research2024
Instability throughout the Saccharomyces cerevisiae genome resulting from Pms1 endonuclease deficiency.
Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Two distinct Okazaki fragment failure modes dominate mutagenesis in the absence of flap endonuclease 1.Nature communications · 2026Article
- Genomic Instability and Adaptive Evolution Induced by RFA Insufficiency inCurrent issues in molecular biology · 2026Article
- Evidence that transient replication errors initiate nuclear genome mutations.Nucleic acids research · 2025Article
- Functions of PMS2 and MLH1 important for regulation of divergent repeat-mediated deletions.DNA repair · 2025Article
- Action-At-A-Distance in DNA Mismatch Repair: Mechanistic Insights and Models for How DNA and Repair Proteins Facilitate Long-Range Communication.Biomolecules · 2024Review
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Authors and funding
5 authors.
Funding
Abstract
The endonuclease activity of Pms1 directs mismatch repair by generating a nick in the newly replicated DNA strand. Inactivating Pms2, the human homologue of yeast Pms1, increases the chances of colorectal and uterine cancers. Here we use whole genome sequencing to show that loss of this endonuclease activity, via the pms1-DE variant, results in strong mutator effects throughout the Saccharomyces cerevisiae genome. Mutation rates are strongly increased for mutations resulting from all types of single-base substitutions and for a wide variety of single- and multi-base indel mutations. Rates for these events are further increased in strains combining pms1-DE with mutator variants of each of the three major leading and lagging strand replicases. In all cases, mutation rates, spectra, biases, and context preferences are statistically indistinguishable from strains with equivalent polymerases but lacking initial mismatch recognition due to deletion of MSH2. This implies that, across the nuclear genome, strand discrimination via the Pms1 endonuclease is as important for MMR as is initial mismatch recognition by Msh2 heterodimers.
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Registered trials
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