复制后修复
生物
大肠杆菌
DNA修复
遗传学
细胞生物学
DNA
基因
DNA错配修复
作者
Michael M. Cox,Myron F. Goodman,James L. Keck,Antoine M. van Oijen,Susan T. Lovett,Andrew Robinson
标识
DOI:10.1128/mmbr.00078-22
摘要
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.
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