期刊
DNA REPAIR
卷 56, 期 -, 页码 118-128出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.dnarep.2017.06.014
关键词
DNA replication; Genetic recombination; Mutagenesis; Copy number variation; Quasipalindrome; Postreplication repair
资金
- [R01 GM51753]
- [P01 GM105473]
Replication forks frequently are challenged by lesions on the DNA template, replication-impeding DNA secondary structures, tightly bound proteins or nucleotide pool imbalance. Studies in bacteria have suggested that under these circumstances the fork may leave behind single-strand DNA gaps that are subsequently filled by homologous recombination, translesion DNA synthesis or template-switching repair synthesis. This review focuses on the template-switching pathways and how the mechanisms of these processes have been deduced from biochemical and genetic studies. I discuss how template-switching can contribute significantly to genetic instability, including mutational hotspots and frequent genetic rearrangements, and how template-switching may be elicited by replication fork damage.
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