Break-Induced Replication: The Where, The Why, and The How.

Break-Induced Replication: The Where, The Why, and The How.
复制标题

突破引起的复制:在哪里,原因和方式。

DOI:
10.1016/j.tig.2018.04.002
复制
发表时间:
2018-07
期刊:
Trends in genetics : TIG
影响因子:
--
通讯作者:
Malkova A
Malkova A
中科院分区:
其他
文献类型:
--
作者:
Kramara J;Osia B;Malkova A

文献摘要

参考文献

被引文献

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断裂诱导复制(BIR)是一种修复单端双链断裂(DSB)的途径。几十年来,酵母模型系统提供了研究真核生物BIR的唯一机会。这些研究描述了一种不寻常的BIR合成模式,该模式通过迁移气泡进行,并显示新合成DNA的保守遗传,导致基因组不稳定性,如与人类癌症相关的基因组不稳定性。然而,BIR在哺乳动物或其他DNA断裂修复过程中发挥作用的证据一直缺失。最近的研究发现了BIR在酵母和哺乳动物中复制重启和修复受损端粒的多个例子,以及一些意想不到的发现,包括BIR的RAD 51独立性。强烈的兴趣仍然是确定在不同的遗传背景下,跨生物体,特别是在人类疾病的背景下,驱动和调节BIR的分子机制的变化。
Break induced replication (BIR) is a pathway that repairs one-ended double strand breaks (DSBs). For decades, yeast model systems offered the only opportunities to study eukaryotic BIR. These studies described an unusual mode of BIR synthesis that is carried out by a migrating bubble and shows conservative inheritance of newly synthesized DNA, leading to genomic instabilities like those associated with cancer in humans. Yet, evidence of BIR functioning in mammals or during repair of other DNA breaks has been missing. Recent studies have uncovered multiple examples of BIR working in replication restart and repair of eroded telomeres in yeast and mammals as well as some unexpected findings, including the RAD51 independence of BIR. Strong interest remains in determining the variations in molecular mechanisms that drive and regulate BIR in different genetic backgrounds, across organisms, and particularly in the context of human disease.
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