GSE194101
Role of H3K36 methylation in regulating transcription coupled-nucleotide excision repair
We characterized the role of H3K36 methylation in regulating repair of UV damage from the transcribed strand (TS) of yeast genes by the transcription coupled nucleotide excision repair (TC-NER) pathway. TC-NER is triggered when RNA polymerase stalls at UV damage, such as a UV-induced cyclobutane pyrimidine dimer (CPD). During transcription, the histone methyltransferase Set2 methylates histone H3K36, but it is not known if H3K36 methylation regulates TC-NER. Here, we report genome-wide repair maps of UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast cells containing mutants in histone H3K36 (or set2). Overall design: UV-induced CPD lesions were mapped in yeast cells both immediately after UV damage formation (0hr time point) and following two hours of repair (2hr time point) using the CPD-seq method. Repair of CPD lesions was measured in yeast cells mutated in the histone H3 gene (H3K36A) or a WT control. Repair was also analyzed in rad16?H3K36A or rad16set2? double mutants, which is deficient in the global genomic NER (GG-NER) pathway.