DNA聚合酶UmuC家族的翻译合成

Zhigang Wang
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引用次数: 90

摘要

翻译合成是克服DNA损伤阻断复制的重要细胞机制。为了在复制过程中复制受损的DNA模板,需要专门的DNA聚合酶。平移合成可以是无错误的,也可以是容易出错的。从大肠杆菌到人类,易出错的翻译合成构成了DNA损伤诱导突变的主要机制。作为对复制过程中DNA损伤的反应,翻译合成有助于细胞存活和诱导诱变。1999-2000年间,UmuC超家族已经出现,它由以下原型成员组成:大肠杆菌UmuC、大肠杆菌DinB、酵母Rad30、人类RAD30B和酵母Rev1。相应的生化活性分别为DNA聚合酶V、IV、η、ι和dCMP转移酶。本文对UmuC超家族的最新研究进行了总结,并提出证据表明该DNA聚合酶家族参与翻译DNA合成。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Translesion synthesis by the UmuC family of DNA polymerases

Translesion synthesis is an important cellular mechanism to overcome replication blockage by DNA damage. To copy damaged DNA templates during replication, specialized DNA polymerases are required. Translesion synthesis can be error-free or error-prone. From E. coli to humans, error-prone translesion synthesis constitutes a major mechanism of DNA damage-induced mutagenesis. As a response to DNA damage during replication, translesion synthesis contributes to cell survival and induced mutagenesis. During 1999–2000, the UmuC superfamily had emerged, which consists of the following prototypic members: the E. coli UmuC, the E. coli DinB, the yeast Rad30, the human RAD30B, and the yeast Rev1. The corresponding biochemical activities are DNA polymerases V, IV, η, ι, and dCMP transferase, respectively. Recent studies of the UmuC superfamily are summarized and evidence is presented suggesting that this family of DNA polymerases is involved in translesion DNA synthesis.

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