同源重组
生物
DNA修复
DNA
突变
复制蛋白A
同源染色体
遗传学
综合征如奈梅亨破损综合症
DNA复制
DNA损伤
非同源性末端接合
同源定向修复
细胞生物学
突变
DNA错配修复
基因
DNA结合蛋白
共济失调毛细血管扩张
转录因子
作者
Lepakshi Ranjha,Sean Howard,Petr Ćejka
出处
期刊:Chromosoma
[Springer Science+Business Media]
日期:2018-01-11
卷期号:127 (2): 187-214
被引量:305
标识
DOI:10.1007/s00412-017-0658-1
摘要
DNA double-strand breaks arise accidentally upon exposure of DNA to radiation and chemicals or result from faulty DNA metabolic processes. DNA breaks can also be introduced in a programmed manner, such as during the maturation of the immune system, meiosis, or cancer chemo- or radiotherapy. Cells have developed a variety of repair pathways, which are fine-tuned to the specific needs of a cell. Accordingly, vegetative cells employ mechanisms that restore the integrity of broken DNA with the highest efficiency at the lowest cost of mutagenesis. In contrast, meiotic cells or developing lymphocytes exploit DNA breakage to generate diversity. Here, we review the main pathways of eukaryotic DNA double-strand break repair with the focus on homologous recombination and its various subpathways. We highlight the differences between homologous recombination and end-joining mechanisms including non-homologous end-joining and microhomology-mediated end-joining and offer insights into how these pathways are regulated. Finally, we introduce noncanonical functions of the recombination proteins, in particular during DNA replication stress.
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