Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Department of Biological Sciences, University of Southern California, University Park, Los Angeles, California, USA.
Microbiol Mol Biol Rev. 2023 Jun 28;87(2):e0007822. doi: 10.1128/mmbr.00078-22. Epub 2023 May 22.
When replication forks encounter template lesions, one result is lesion skipping, where the stalled DNA polymerase transiently stalls, disengages, and then reinitiates downstream to leave the lesion behind in a postreplication gap. Despite considerable attention in the 6 decades since postreplication gaps were discovered, the mechanisms by which postreplication gaps are generated and repaired remain highly enigmatic. This review focuses on postreplication gap generation and repair in the bacterium Escherichia coli. New information to address the frequency and mechanism of gap generation and new mechanisms for their resolution are described. There are a few instances where the formation of postreplication gaps appears to be programmed into particular genomic locations, where they are triggered by novel genomic elements.
当复制叉遇到模板损伤时,一种结果是损伤跳过,其中停滞的 DNA 聚合酶暂时停滞,脱离,并在下游重新起始,从而将损伤留在复制后缺口(postreplication gap)中。尽管自复制后缺口被发现以来的 60 多年来已经引起了相当多的关注,但复制后缺口的产生和修复机制仍然非常神秘。本综述重点介绍了细菌大肠杆菌中的复制后缺口的产生和修复。描述了新的信息来解决缺口产生的频率和机制,以及解决它们的新机制。在某些情况下,复制后缺口的形成似乎被编程到特定的基因组位置,在这些位置,它们被新的基因组元件触发。