Mismatch Repair Mutants in Yeast Are Not Defective in Transcription-Coupled DNA Repair of UV-Induced DNA Damage

摘要

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 Δ mutants. We also determined whether the Rad26-independent transcription-coupled repair observed in rad26 Δ and rad7Δ rad26 Δ mutants depends on MSH2 by examining repair deficiencies of rad26Δ msh2 Δ and rad7Δ rad26Δ msh2 Δ 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.