The DNA mismatch repair (MMR) system is a major DNA repair pathway whose function is critical for the correction of
DNA biosynthetic errors. MMR is initiated by the binding of
MutS proteins to mismatches and unpaired
nucleotides followed by the recruitment of
MutL proteins. The major MutL activity in eukaryotes is performed by MutLĪ±, the heterocomplex of MLH1-PMS1 in yeast and plants and MLH1-PMS2 in humans. We here report the effect the expression of
Arabidopsis PMS1 protein exerts on Saccharomyces cerevisiae
genomic stability. A strain carrying specific
microsatellite instability reporter systems was chosen for the study. The
plant protein failed to
complement the hypermutator phenotype of a pms1 deficient strain but increased approximately 14-fold and 2,000-fold the mutation rates of his7-2 and lys2::InsE-A 14 loci of MMR proficient strains when compared to wild-type strains, respectively. Overexpressing AtMLH1 in the AtPMS1-overproducing strain generated an increase in mutation rate comparable to that of AtPMS1 expression alone. Deletion of the C-terminal residues implicated in
protein-
protein interaction and including the putative
endonuclease sequence of AtPMS1 completely eliminated the mutator phenotype. Taken together, these results indicate that the
plant proteins affect yeast
genomic stability, very possibly altering
protein-
protein interactions that are necessary to complete repair.