Epshtein Vitaliy
Department of Biochemistry, New York University, Langhorn Medical Center, New York, NY, USA.
Bioessays. 2015 Jan;37(1):12-9. doi: 10.1002/bies.201400106. Epub 2014 Oct 27.
Transcription-coupled repair (TCR) is a phenomenon that exists in a wide variety of organisms from bacteria to humans. This mechanism allows cells to repair the actively transcribed DNA strand much faster than the non-transcribed one. At the sites of bulky DNA damage RNA polymerase stalls, initiating recruitment of the repair machinery. It is a commonly accepted paradigm that bacterial cells utilize a sole coupling factor, called Mfd to initiate TCR. According to that model, Mfd removes transcription complexes stalled at the lesion site and simultaneously recruits repair machinery. However, this model was recently put in doubt by various discrepancies between the proposed universal role of Mfd in the TCR and its biochemical and phenotypical properties. Here, I present a second pathway of bacterial TCR recently discovered in my laboratory, which does not involve Mfd but implicates a common repair factor, UvrD, in a central position in the process.
转录偶联修复（TCR）是一种存在于从细菌到人类等多种生物体中的现象。这种机制使细胞能够比未转录的DNA链更快地修复正在被积极转录的DNA链。在DNA发生大片段损伤的位点，RNA聚合酶会停滞，从而启动修复机制的募集。细菌细胞利用一种名为Mfd的单一偶联因子来启动TCR，这是一个被广泛接受的范式。根据该模型，Mfd移除在损伤位点停滞的转录复合物，并同时募集修复机制。然而，最近TCR中Mfd的普遍作用与其生化和表型特性之间存在的各种差异对该模型提出了质疑。在此，我介绍我实验室最近发现的细菌TCR的第二条途径，该途径不涉及Mfd，但涉及一种常见的修复因子UvrD，它在这一过程中处于核心地位。
