Genome Damage and Stability Centre, School of Life Sciences, University of Sussex, Brighton BN1 9RQ, UK.
J Mol Biol. 2013 Nov 29;425(23):4733-44. doi: 10.1016/j.jmb.2013.04.023. Epub 2013 Apr 30.
Homologous recombination (HR) is an evolutionary-conserved mechanism involved in a subtle balance between genome stability and diversity. HR is a faithful DNA repair pathway and has been largely characterized in the context of double-strand break (DSB) repair. Recently, multiple functions for the HR machinery have been identified at arrested forks. These are evident across different organisms and include replication fork-stabilization and fork-restart functions. Interestingly, a DSB appears not to be a prerequisite for HR-mediated replication maintenance. HR has the ability to rebuild a replisome at inactivated forks, but perhaps surprisingly, the resulting replisome is liable to intrastrand and interstrand switches leading to replication errors. Here, we review our current understanding of the replication maintenance function of HR. The error proneness of these pathways leads us to suggest that the origin of replication-associated genome instability should be re-evaluated.
同源重组（HR）是一种进化上保守的机制，涉及基因组稳定性和多样性之间的微妙平衡。HR 是一种忠实的 DNA 修复途径，在双链断裂（DSB）修复的背景下已得到广泛研究。最近，在停滞的叉路口发现了 HR 机制的多种功能。这些功能在不同的生物体中都很明显，包括复制叉稳定和叉重新启动功能。有趣的是，DSB 似乎不是 HR 介导的复制维持的先决条件。HR 有能力在失活的叉路口重建复制体，但也许令人惊讶的是，由此产生的复制体容易发生链内和链间转换，导致复制错误。在这里，我们回顾了我们对 HR 的复制维持功能的现有认识。这些途径的易错性使我们建议应该重新评估与复制起点相关的基因组不稳定性的起源。
