Instability throughout the Saccharomyces cerevisiae genome resulting from Pms1 endonuclease deficiency.

Abstract excerpt

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...

Topics

Join the communities discussing this publication.

• DNA Mismatch Repair
• Genome, Fungal
• Genomic Instability
• Mutation Rate
• MutL Proteins