Cancer Research Center of Marseille, CNRS, UMR7258; Genome Instability and Carcinogenesis (equipe labellisée Ligue Contre le Cancer) Inserm, U1068; Paoli-Calmettes Institute, Aix-Marseille Université, F-13009 Marseille, France.
Cold Spring Harb Perspect Biol. 2013 Dec 1;5(12):a012682. doi: 10.1101/cshperspect.a012682.
The presence of unrepaired lesions in DNA represents a challenge for replication. Most, but not all, DNA lesions block the replicative DNA polymerases. The conceptually simplest procedure to bypass lesions during DNA replication is translesion synthesis (TLS), whereby the replicative polymerase is transiently replaced by a specialized DNA polymerase that synthesizes a short patch of DNA across the site of damage. This process is inherently error prone and is the main source of point mutations. The diversity of existing DNA lesions and the biochemical properties of Escherichia coli DNA polymerases will be presented. Our main goal is to deliver an integrated view of TLS pathways involving the multiple switches between replicative and specialized DNA polymerases and their interaction with key accessory factors. Finally, a brief glance at how other bacteria deal with TLS and mutagenesis is presented.
DNA 中未修复的损伤的存在对复制构成了挑战。大多数（但不是全部）DNA 损伤会阻止复制性 DNA 聚合酶。在 DNA 复制过程中绕过损伤的概念上最简单的方法是跨损伤合成（TLS），其中复制性聚合酶被专门的 DNA 聚合酶短暂取代，该聚合酶在损伤部位合成一小段 DNA。这个过程本质上是易错的，是点突变的主要来源。我们将介绍现有的多种 DNA 损伤和大肠杆菌 DNA 聚合酶的生化特性。我们的主要目标是提供一个综合的 TLS 途径视图，包括复制性和专门性 DNA 聚合酶之间的多个开关及其与关键辅助因子的相互作用。最后，简要介绍了其他细菌如何处理 TLS 和突变。
