作者: Susan T. Lovett
DOI: 10.1016/J.DNAREP.2017.06.014
关键词:
摘要: Replication forks frequently are challenged by lesions on the DNA template, replication-impeding secondary structures, tightly bound proteins or nucleotide pool imbalance. Studies in bacteria have suggested that under these circumstances fork may leave behind single-strand gaps subsequently filled homologous recombination, translesion synthesis template-switching repair synthesis. This review focuses pathways and how mechanisms of processes been deduced from biochemical genetic studies. I discuss can contribute significantly to instability, including mutational hotspots frequent rearrangements, be elicited replication damage.