One-ended and two-ended breaks at nickase-broken replication forks

IF 3 3区 生物学 Q2 GENETICS & HEREDITY DNA Repair Pub Date : 2024-11-04 DOI:10.1016/j.dnarep.2024.103783
Ralph Scully , Johannes C. Walter , André Nussenzweig
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Abstract

Replisome collision with a nicked parental DNA template can lead to the formation of a replication-associated double strand break (DSB). How this break is repaired has implications for cancer initiation, cancer therapy and therapeutic gene editing. Recent work shows that collision of a replisome with a nicked DNA template can give rise to either a single-ended (se) or a double-ended (de)DSB, with potentially divergent effects on repair pathway choice and genomic instability. Emerging evidence suggests that the biochemical environment of the broken mammalian replication fork may be specialized in such a way as to skew repair in favor of homologous recombination at the expense of non-homologous end joining.
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缺口酶断裂复制叉上的单端断裂和双端断裂
复制体与有缺口的亲代 DNA 模板碰撞会形成与复制相关的双链断裂(DSB)。如何修复这种断裂对癌症的诱发、癌症治疗和治疗性基因编辑都有影响。最近的研究表明,复制体与切口 DNA 模板的碰撞可产生单端(se)或双端(de)DSB,对修复途径选择和基因组不稳定性可能产生不同的影响。新出现的证据表明,哺乳动物复制叉断裂的生化环境可能具有特异性,以牺牲非同源末端连接为代价,偏向于同源重组修复。
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来源期刊
DNA Repair
DNA Repair 生物-毒理学
CiteScore
7.60
自引率
5.30%
发文量
91
审稿时长
59 days
期刊介绍: DNA Repair provides a forum for the comprehensive coverage of DNA repair and cellular responses to DNA damage. The journal publishes original observations on genetic, cellular, biochemical, structural and molecular aspects of DNA repair, mutagenesis, cell cycle regulation, apoptosis and other biological responses in cells exposed to genomic insult, as well as their relationship to human disease. DNA Repair publishes full-length research articles, brief reports on research, and reviews. The journal welcomes articles describing databases, methods and new technologies supporting research on DNA repair and responses to DNA damage. Letters to the Editor, hot topics and classics in DNA repair, historical reflections, book reviews and meeting reports also will be considered for publication.
期刊最新文献
Discovery of KPT-6566 as STAG1/2 Inhibitor sensitizing PARP and NHEJ Inhibitors to suppress tumor cells growth in vitro Intersection of the fragile X-related disorders and the DNA damage response One-ended and two-ended breaks at nickase-broken replication forks Transient HR enhancement by RAD51-stimulatory compound confers protection on intestinal rather than hematopoietic tissue against irradiation in mice 53BP1-the ‘Pandora’s box’ of genome integrity
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