Hochegger Helfrid, Sonoda Eichiro, Takeda Shunichi
Department of Radiation Genetics, Faculty of Medicine, Kyoto University, Sakyo-ku, 606-8501 Kyoto, Japan.
Bioessays. 2004 Feb;26(2):151-8. doi: 10.1002/bies.10403.
Replication forks inevitably stall at damaged DNA in every cell cycle. The ability to overcome DNA lesions is an essential feature of the replication machinery. A variety of specialized polymerases have recently been discovered, which enable cells to replicate past various forms of damage by a process termed translesion synthesis. Alternatively, homologous recombination can be used to restart DNA replication across the lesion. Genetic and biochemical studies have shed light on the impact of these two post-replication repair pathways in bacteria and yeast. In vertebrates, however, a genetic approach to study post-replication repair has been compromised because many of the genes involved appear to be essential for embryonic development. We have taken advantage of the chicken cell line DT40 to perform a genetic analysis of translesion synthesis and homologous recombination and to characterize genetic interactions between these two pathways in vertebrates. In this article, we aim to summarize our current understanding of post-replication repair in DT40 in the perspective of bacterial, yeast and mammalian genetics.
在每个细胞周期中，复制叉不可避免地会在受损的DNA处停滞。克服DNA损伤的能力是复制机制的一个基本特征。最近发现了多种特殊的聚合酶，它们使细胞能够通过一种称为跨损伤合成的过程复制通过各种形式的损伤。另外，同源重组可用于重新启动跨越损伤的DNA复制。遗传和生化研究揭示了这两种复制后修复途径在细菌和酵母中的影响。然而，在脊椎动物中，由于许多涉及的基因似乎对胚胎发育至关重要，研究复制后修复的遗传方法受到了限制。我们利用鸡细胞系DT40对跨损伤合成和同源重组进行遗传分析，并表征脊椎动物中这两种途径之间的遗传相互作用。在本文中，我们旨在从细菌、酵母和哺乳动物遗传学的角度总结我们目前对DT40中复制后修复的理解。
