Role of Set2 in regulating transcription coupled-nucleotide excision repair

Repair of UV damage from the transcribed strand (TS) of yeast genes is rapid due to 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 Set2 regulates TC-NER. Here, we report genome-wide repair maps of UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast cells lacking Set2.酵母基因的转录链（transcribed strand，TS）上的紫外线损伤修复可通过转录偶联核苷酸切除修复（transcription coupled nucleotide excision repair，TC-NER）通路快速完成。当RNA聚合酶（RNA polymerase）停滞于紫外线诱导的环丁烷嘧啶二聚体（UV-induced cyclobutane pyrimidine dimer，CPD）这类紫外线损伤位点时，TC-NER通路即被触发。转录过程中，组蛋白甲基转移酶Set2（histone methyltransferase Set2）会对组蛋白H3K36进行甲基化修饰，但目前尚不清楚Set2是否可调控TC-NER通路。本研究针对缺失Set2的酵母细胞，生成了紫外线诱导的环丁烷嘧啶二聚体（CPD）的全基因组修复图谱。