Repair of DNA Breaks by Break-Induced Replication.
Repair of DNA Breaks by Break-Induced Replication.
复制标题
通过断裂诱导复制修复 DNA 断裂。
DOI：
10.1146/annurev-biochem-081420-095551
复制
发表时间：
2021-06-20
影响因子：
16.6
通讯作者：
中科院分区：
文献类型：
--
作者：
双链DNA断裂（DSB）是最致命的DNA损伤类型，使DSB修复对细胞存活至关重要。然而，一些DSB修复途径是致突变的，并促进基因组重排，导致基因组不稳定。其中一种途径是断裂诱导的复制，它主要修复一端的DSB，类似于由折叠的复制叉或端粒侵蚀形成的DSB。BIR由断裂的DNA末端侵入同源模板而启动，在迁移气泡的背景下合成新的DNA，并且与新遗传物质的保守遗传有关。这种合成模式是与BIR相关的高水平遗传不稳定性的原因。真核生物BIR最初是在酵母中研究的，但现在也通过使用报告基因和研究端粒的替代延长来积极研究哺乳动物系统。此外，我们对微同源介导的BIR在形成复杂基因组重排中的作用的理解也取得了重大突破，这些基因组重排是各种人类病理学的基础，包括神经系统疾病和癌症。
Double-strand DNA breaks (DSB) are the most lethal type of DNA damage, making DSB repair critical for cell survival. However, some DSB repair pathways are mutagenic and promote genome rearrangements, leading to genome destabilization. One such pathway is break-induced replication, which repairs primarily one-ended DSBs, similar to those formed by collapsed replication forks or by telomere erosion. BIR is initiated by invasion of a broken DNA end into a homologous template, synthesizes new DNA within the context of a migrating bubble, and is associated with conservative inheritance of new genetic material. This mode of synthesis is responsible for a high level of genetic instability associated with BIR. Eukaryotic BIR was initially investigated in yeast, but now it is also actively studied in mammalian systems by employing reporters, and by investigating alternative lengthening of telomeres. Additionally, a significant breakthrough has been made in our understanding of the role of microhomology-mediated BIR in the formation of complex genomic rearrangements that underly various human pathologies, including neurological diseases and cancer.
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影响因子：
4.5
作者：
Chung WH;Zhu Z;Papusha A;Malkova A;Ira G
通讯作者：
Ira G
影响因子：
16.6
作者：
Arora, Rajika;Lee, Yongwoo;Wischnewski, Harry;Brun, Catherine M.;Schwarz, Tobias;Azzalin, Claus M.
通讯作者：
Azzalin, Claus M.
影响因子：
11.4
作者：
ASAI, T;SOMMER, S;KOGOMA, T
通讯作者：
KOGOMA, T
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64.5
作者：
ASAI, T;BATES, DB;KOGOMA, T
通讯作者：
KOGOMA, T
影响因子：
11.4
作者：
BRYAN, TM;ENGLEZOU, A;REDDEL, RR
通讯作者：
REDDEL, RR