Ross S L, Sharma S, Moses R E
Mol Gen Genet. 1980;179(3):595-605. doi: 10.1007/BF00271750.
Bleomycin (BLM) is an antitumor drug which interacts with and damages DNA. We have reported a repair response dependent on DNA polymerase I in toluene-treated Escherichia coli. We report here that DNA polymerase III can also catalyze a repair response in toluene-treated E. coli following exposure to BLM. Polymerase III-mediated synthesis differs because it is ATP-dependent, whereas polymerase I-mediated repair synthesis is not. Polymerase III repair synthesis is independent of replicative synthesis, as demonstrated in a polA-, dnaBts strain, or use of Novobiocin to inhibit replication, and replication persists in the presence of repair synthesis. It appears that ATP-dependent repair synthesis in response to BLM is also present in polA+ strains. Repair synthesis does not require the uvrA gene product.
博来霉素(BLM)是一种与DNA相互作用并损伤DNA的抗肿瘤药物。我们曾报道在经甲苯处理的大肠杆菌中存在一种依赖于DNA聚合酶I的修复反应。我们在此报告,在经甲苯处理的大肠杆菌暴露于BLM后,DNA聚合酶III也能催化修复反应。聚合酶III介导的合成有所不同,因为它依赖于ATP,而聚合酶I介导的修复合成则不依赖ATP。聚合酶III修复合成独立于复制合成,这在polA -、dnaBts菌株中得到证明,或者使用新生霉素抑制复制时也可证明,并且在存在修复合成的情况下复制仍持续进行。似乎在polA +菌株中也存在对BLM的依赖于ATP的修复合成。修复合成不需要uvrA基因产物。