Regulation and rate enhancement during transcription-coupled DNA repair.
Regulation and rate enhancement during transcription-coupled DNA repair.
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DOI：
10.1016/j.molcel.2010.11.012
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发表时间：
2010-12-10
期刊：
影响因子：
16
通讯作者：
Savery NJ
中科院分区：
文献类型：
--
作者：
Manelyte L;Kim YI;Smith AJ;Smith RM;Savery NJ
转录偶联DNA修复(TCR)是核苷酸切除修复(NER)的一个子途径，当RNA聚合酶因DNA损伤而停滞时被触发。TCR靶向的损伤比转录非依赖的“全局”NER途径修复的损伤更快，但这种速率提高的机制尚不清楚。细菌NER过程中的损伤识别依赖于UvrA，它与损伤结合并将UvrB加载到DNA上。细菌TCR还需要MFD蛋白，这是一种DNA转位酶，可以移除停滞的转录复合体。我们已经确定了在TCR期间观察到的高修复率所需的MFD、UvrA和UvrB的性质。我们发现TCR和全局NER对UvrA损伤识别的要求不同，表明MFD在修复过程的最早阶段起作用，并扩大了细菌和真核生物中TCR之间的功能相似性。►细菌的TCR绕过了UvrA►对损伤识别的需要，Mfd的UvrB同源模块负责链特异性修复►，大肠杆菌UvrA的插入结构域参与损伤识别►域间接触调节Mfd的活性
Transcription-coupled DNA repair (TCR) is a subpathway of nucleotide excision repair (NER) that is triggered when RNA polymerase is stalled by DNA damage. Lesions targeted by TCR are repaired more quickly than lesions repaired by the transcription-independent “global” NER pathway, but the mechanism underlying this rate enhancement is not understood. Damage recognition during bacterial NER depends upon UvrA, which binds to the damage and loads UvrB onto the DNA. Bacterial TCR additionally requires the Mfd protein, a DNA translocase that removes the stalled transcription complexes. We have determined the properties of Mfd, UvrA, and UvrB that are required for the elevated rate of repair observed during TCR. We show that TCR and global NER differ in their requirements for damage recognition by UvrA, indicating that Mfd acts at the very earliest stage of the repair process and extending the functional similarities between TCR in bacteria and eukaryotes. ► Bacterial TCR bypasses the need for damage recognition by UvrA ► The UvrB homology module of Mfd is responsible for strand-specific repair ► The insertion domain of E. coli UvrA is involved in damage recognition ► Interdomain contacts regulate the activity of Mfd
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