Defects in DNA mismatch repair have been shown to lead to increased genomic 
instability and mutability. We recently found that human cells defective in the 
DNA mismatch repair gene, hMSH2, were deficient in the transcription-coupled 
repair (TCR) of both oxidative DNA damage, including thymine glycols, and 
UV-induced DNA damage. However, in a hMLH1 mutant, only a reduction in the TCR 
of UV damage was observed. In this study, we examined whether TCR of thymine 
glycols in Saccharomyces cerecisiae also requires the genes involved in DNA 
mismatch repair. We found that yeast cells containing mutations in MSH2 were 
deficient in the removal of thymine glycols from the transcribed strand of the 
RPB2 gene, while cells with mutations in either MLH1 or PMS1 alone showed near 
normal levels of TCR of thymine glycols. Interestingly, double mutants in the 
MLH1 and PMS1 genes were deficient in TCR of thymine glycols. Taken together, 
these results suggest that these two MutL homologues can act independently of 
each other, but that they have overlapping roles in TCR. Overall levels of 
thymine glycol removal were not reduced in the mismatch repair mutants. In 
contrast to the results with thymine glycols, no defects in TCR of pyrimidine 
dimers were found in cells with mutations in MSH2, MLH1, PMS1, and MLH1/PMS1.