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Colloquium Paper: Roles of DNA polymerases V and II in SOS-induced error-prone and error-free repair in Escherichia coli

机译:专题讨论会:DNA聚合酶V和II在大肠杆菌中易受SOS诱导的易错和无错修复中的作用

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摘要

DNA polymerase V, composed of a heterotrimer of the DNA damage-inducible UmuC and UmuD proteins, working in conjunction with RecA, single-stranded DNA (ssDNA)-binding protein (SSB), β sliding clamp, and γ 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 (≈2 min post-UV irradiation), whereas TLS occurs after pol V is induced ≈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.
机译:DNA聚合酶V是由DNA损伤诱导型UmuC和UmuD蛋白的异源三聚体组成,与RecA,单链DNA(ssDNA)结合蛋白(SSB),β滑动钳和γ钳装载复合物共同作用。通过催化跨病变合成(TLS)负责大肠杆菌中大多数SOS病变靶向突变。 DNA聚合酶II是损伤诱导型polB(dinA)基因的产物,在复制-重新启动过程中起着关键作用,该过程以无错误的方式绕过了DNA损伤。复制重启几乎在DNA受损后立即发生(紫外线照射后约2分钟),而TLS发生在约50分钟后诱导pol V之后。我们讨论pol V催化TLS和pol II催化的复制重启的最新数据。最近已确定TLS V在TLS期间的特定角色及其每个辅助因素。尽管仍未阐明pol II依赖性复制-重新启动的确切分子机制,但最近已证明它可与RecFOR和PriA蛋白结合使用。

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