DNA replication: the recombination connection.

DNA replication: the recombination connection.
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DOI:
10.1016/j.tcb.2021.07.005
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发表时间:
2022-01
影响因子:
19
通讯作者:
Haber JE
Haber JE
中科院分区:
生物学1区
文献类型:
--
作者:
Epum EA;Haber JE

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不能完成DNA复制是基因组不稳定性的主要来源之一,其导致与人类癌症相关的非整倍性、染色体断裂和染色体重排。过去十年中令人惊讶的发现之一是,在所谓的常见脆性位点完成复制发生在细胞周期的很晚阶段-在有丝分裂-通过称为MiDAS(有丝分裂DNA合成)的过程。MiDAS已被证明与另一种促癌现象密切相关:端粒替代延长(ALT)机制的激活。我们对哺乳动物细胞中ALT和MiDAS的机制的理解在很大程度上来自于最近在断裂诱导复制(BIR)特别是芽殖酵母中的研究进展。在这里,我们提供了关于BIR,MiDAS和ALT途径及其共同相似性的新见解。
The failure to complete DNA replication is one of the major sources of genome instability that leads to aneuploidy, chromosome breakage, and chromosome rearrangements associated with human cancer. One of the surprising revelations of the past decade is that the completion of replication at so-called common fragile sites occurs very late in the cell cycle – at mitosis – through a process termed MiDAS (mitotic DNA synthesis). MiDAS has proven to be strongly related to another cancer-promoting phenomenon: the activation of alternative lengthening of telomeres (ALT) mechanisms. Our understanding of the mechanisms of ALT and MiDAS in mammalian cells has drawn heavily from recent advances in the study of break-induced replication (BIR) especially in budding yeast. Here we provide new insights on BIR, MiDAS and ALT pathways and their shared similarities.
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