Replication fork reversal and the maintenance of genome stability.
Replication fork reversal and the maintenance of genome stability.
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DOI：
10.1093/nar/gkp244
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发表时间：
2009-06
影响因子：
14.9
通讯作者：
McGlynn P
中科院分区：
文献类型：
--
作者：
Atkinson J;McGlynn P
复制叉的进展在体内经常受到DNA损伤和与模板结合的蛋白质的威胁。为了完成基因组复制，被阻塞的分叉必须以某种方式重新启动，并且最初的阻塞被清除，这意味着被阻塞的分叉处理可能对基因组稳定性至关重要。一种可能的途径，可能允许处理和重新启动的封锁叉，复制叉逆转，涉及解开封锁叉形成四链结构类似霍利迪结。这一概念最近越来越受欢迎，基于这种处理的能力，以解释许多遗传观察，在体内检测未缠绕的叉结构和鉴定有能力在体外催化叉退化的酶。在这里，我们讨论的背景下，叉回归可能会发生，可能会促进这种反应的因素和复制叉解旋在正常的DNA代谢中可能发挥的作用。
The progress of replication forks is often threatened in vivo, both by DNA damage and by proteins bound to the template. Blocked forks must somehow be restarted, and the original blockage cleared, in order to complete genome duplication, implying that blocked fork processing may be critical for genome stability. One possible pathway that might allow processing and restart of blocked forks, replication fork reversal, involves the unwinding of blocked forks to form four-stranded structures resembling Holliday junctions. This concept has gained increasing popularity recently based on the ability of such processing to explain many genetic observations, the detection of unwound fork structures in vivo and the identification of enzymes that have the capacity to catalyse fork regression in vitro. Here, we discuss the contexts in which fork regression might occur, the factors that may promote such a reaction and the possible roles of replication fork unwinding in normal DNA metabolism.
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