Transcription-coupled repair (TCR), discovered as preferential nucleotide excision repair of UV-induced cyclobutane pyrimidine dimers located in transcribed mammalian genes compared to those in nontranscribed regions of the genome, is defined as faster repair of the transcribed strand versus the nontranscribed strand in transcribed genes. The phenomenon, universal in model organisms including Escherichia coli, yeast, Arabidopsis, mice, and humans, involves a translocase that interacts with both RNA polymerase stalled at damage in the transcribed strand and nucleotide excision repair proteins to accelerate repair. Drosophila, a notable exception, exhibits TCR but lacks an obvious TCR translocase. Mutations inactivating TCR genes cause increased damage-induced mutagenesis in E. coli and severe neurological and UV sensitivity syndromes in humans. To date, only E. coli TCR has been reconstituted in vitro with purified proteins. Detailed investigations of TCR using genome-wide next-generation sequencing methods, cryo–electron microscopy, single-molecule analysis, and other approaches have revealed fascinating mechanisms.

中文翻译：

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转录偶联修复的分子机制

转录偶联修复（TCR）被发现是与基因组非转录区域相比，位于转录哺乳动物基因中的紫外线诱导的环丁烷嘧啶二聚体的优先核苷酸切除修复，被定义为转录链相对于非转录链的更快修复转录基因。这种现象在包括大肠杆菌、酵母、拟南芥、小鼠和人类在内的模型生物体中普遍存在，涉及一种转位酶，该转位酶与转录链损伤时停滞的RNA聚合酶和核苷酸切除修复蛋白相互作用，以加速修复。果蝇是一个值得注意的例外，它表现出 TCR，但缺乏明显的 TCR 易位酶。使 TCR 基因失活的突变会导致大肠杆菌损伤诱导突变增加，以及人类严重的神经和紫外线敏感性综合症。迄今为止，只有大肠杆菌 TCR 已在体外用纯化的蛋白质重建。使用全基因组下一代测序方法、冷冻电子显微镜、单分子分析和其他方法对 TCR 进行详细研究揭示了令人着迷的机制。