Mismatch recognition function of Arabidopsis thaliana MutSgamma . Genetic stability depends in part on an efficient DNA lesion recognition and correction by the DNA mismatch repair ( MMR ) system. In eukaryotes , MMR is initiated by the binding of heterodimeric MutS homologue ( MSH ) complexes , MSH2 - MSH6 and MSH2 - MSH3 , which recognize and bind mismatches and unpaired nucleotides . Plants encode another mismatch recognition protein , named MSH7 . MSH7 forms a heterodimer with MSH2 and the protein complex is designated MutSgamma . We here report the effect the expression of Arabidopsis MSH2 and MSH7 alone or in combination exert on the genomic stability of Saccharomyces cerevisiae . AtMSH2 and AtMutSgamma proteins failed to complement the hypermutator phenotype of an msh2 deficient strain . However , overexpressing AtMutSgamma in MMR proficient strains generated a 4 - fold increase in CAN1 forward mutation rate , when compared to wild - type strains . Can ( r ) mutation spectrum analysis of AtMutSgamma overproducing strains revealed a substantial increase in the frequency of base substitution mutations , including an increased accumulation of base pair changes from G : C to A : T and T : A to C : G , G : C or A : T . Taken together , these results suggest that AtMutSgamma affects yeast genomic stability by recognizing specific mismatches and preventing correction by yeast MutSalpha and MutSbeta , with subsequent inability to interact with yeast downstream proteins needed to complete MMR .