Many microsatellite DNA sequences are able to form non-B form DNA secondary structures, such as hairpin loops, cruciforms, triplex DNA or G-quadruplexes. These DNA structures can form a significant impediment to DNA replication and repair, leading to DNA nicks, gaps, and breaks, which can be repaired by homologous recombination (HR). Recent work understanding HR at structure-forming repeats has focused on genetic requirements for replication fork restart, break induced replication (BIR) at broken forks, recombination during and after relocalization of breaks or stalled forks to the nuclear periphery, and how repair pathway choice and kinetics are navigated in the presence of a repeat tract. In this review, we summarize recent developments that illuminate the role of recombination in repairing DNA damage or causing tract length changes within repetitive DNA and its role in maintaining genome stability.

许多微卫星 DNA 序列能够形成非 B 型 DNA 二级结构，例如发夹环、十字形、三链体 DNA 或 G-四链体。这些 DNA 结构可以对 DNA 复制和修复形成重大障碍，导致 DNA 缺口、缺口和断裂，这些可以通过同源重组 (HR) 进行修复。最近了解 HR 在结构形成重复上的工作主要集中在复制叉重新启动的遗传要求、断裂叉处的断裂诱导复制 (BIR)、断裂重新定位期间和之后的重组或停滞的叉到核外围，以及如何选择修复途径和动力学在存在重复道的情况下进行导航。在这篇评论中，