DNA聚合酶V和II在大肠杆菌SOS诱导的易错修复和无错修复中的作用。
Roles of DNA polymerases V and II in SOS-induced error-prone and error-free repair in Escherichia coli.
作者信息
Pham P, Rangarajan S, Woodgate R, Goodman M F
机构信息
Department of Biological Sciences, Hedco Molecular Biology Laboratories, University of Southern California, Los Angeles, CA 90089-1340, USA.
出版信息
Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8350-4. doi: 10.1073/pnas.111007198.
DNA polymerase V, composed of a heterotrimer of the DNA damage-inducible UmuC and UmuD(2)(') proteins, working in conjunction with RecA, single-stranded DNA (ssDNA)-binding protein (SSB), beta sliding clamp, and gamma clamp loading complex, are responsible for most SOS lesion-targeted mutations in Escherichia coli, by catalyzing translesion synthesis (TLS). DNA polymerase II, the product of the damage-inducible polB (dinA ) gene plays a pivotal role in replication-restart, a process that bypasses DNA damage in an error-free manner. Replication-restart takes place almost immediately after the DNA is damaged (approximately 2 min post-UV irradiation), whereas TLS occurs after pol V is induced approximately 50 min later. We discuss recent data for pol V-catalyzed TLS and pol II-catalyzed replication-restart. Specific roles during TLS for pol V and each of its accessory factors have been recently determined. Although the precise molecular mechanism of pol II-dependent replication-restart remains to be elucidated, it has recently been shown to operate in conjunction with RecFOR and PriA proteins.
DNA聚合酶V由DNA损伤诱导型UmuC和UmuD(2)(') 蛋白的异源三聚体组成，与RecA、单链DNA（ssDNA）结合蛋白（SSB）、β滑动夹和γ夹加载复合物协同作用，通过催化跨损伤合成（TLS），负责大肠杆菌中大多数针对SOS损伤的突变。DNA聚合酶II是损伤诱导型polB（dinA）基因的产物，在复制重新启动过程中起关键作用，该过程以无错误的方式绕过DNA损伤。复制重新启动几乎在DNA受损后立即发生（紫外线照射后约2分钟），而TLS在约50分钟后pol V被诱导时发生。我们讨论了pol V催化的TLS和pol II催化的复制重新启动的最新数据。最近已经确定了pol V及其每个辅助因子在TLS过程中的具体作用。尽管pol II依赖性复制重新启动的确切分子机制仍有待阐明，但最近已证明它与RecFOR和PriA蛋白协同作用。
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