Transcription-coupled repair, the targeted repair of the transcribed strands of 
active genes, is defective in bacteria, yeast, and human cells carrying 
mutations in mfd, RAD26 and ERCC6, respectively. Other factors probably are also 
uniquely involved in transcription-repair coupling. Recently, a defect was 
described in transcription-coupled repair for Escherichia coli mismatch repair 
mutants and human tumor cell lines with mutations in mismatch repair genes. We 
examined removal of UV-induced DNA damage in yeast strains mutated in mismatch 
repair genes in an effort to confirm a defect in transcription-coupled repair in 
this system. In addition, we determined the contribution of the mismatch repair 
gene MSH2 to transcription-coupled repair in the absence of global genomic 
repair using rad7 delta mutants. We also determined whether the 
Rad26-independent transcription-coupled repair observed in rad26 delta and rad7 
delta rad26 delta mutants depends on MSH2 by examining repair deficiencies of 
rad26 delta msh2 delta and rad7 delta rad26 delta msh2 delta mutants. We found 
no defects in transcription-coupled repair caused by mutations in the mismatch 
repair genes MSH2, MLH1, PMS1, and MSH3. Yeast appears to differ from bacteria 
and human cells in the capacity for transcription-coupled repair in a mismatch 
repair mutant background.