Thousands of apurinic/apyrimidinic (AP or abasic) sites form in each cell, each day. This simple DNA lesion can have profound consequences to cellular function, genome stability, and disease. As potent blocks to polymerases, they interfere with the reading and copying of the genome. Since they provide no coding information, they are potent sources of mutation. Due to their reactive chemistry, they are intermediates in the formation of lesions that are more challenging to repair including double-strand breaks, interstrand crosslinks, and DNA protein crosslinks. Given their prevalence and deleterious consequences, cells have multiple mechanisms of repairing and tolerating these lesions. While base excision repair of abasic sites in double-strand DNA has been studied for decades, new interest in abasic site processing has come from more recent insights into how they are processed in single-strand DNA. In this review, we discuss the source of abasic sites, their biological consequences, tolerance mechanisms, and how they are repaired in double and single-stranded DNA.

中文翻译：

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对 abasic 位点修复和耐受性的新见解。

每个细胞每天都会形成数千个无嘌呤/无嘧啶（AP 或脱碱基）位点。这种简单的 DNA 损伤可能会对细胞功能、基因组稳定性和疾病产生深远的影响。作为聚合酶的有效阻断剂，它们干扰基因组的读取和复制。由于它们不提供编码信息，因此它们是潜在的突变来源。由于它们的反应性化学性质，它们是损伤形成的中间体，这些损伤更难以修复，包括双链断裂、链间交联和 DNA 蛋白质交联。鉴于其普遍性和有害后果，细胞具有多种修复和耐受这些损伤的机制。虽然双链 DNA 中脱碱基位点的碱基切除修复已经研究了几十年，但对脱碱基位点处理的新兴趣来自于对单链 DNA 中脱碱基位点如何加工的最新见解。在这篇综述中，我们讨论了脱碱基位点的来源、其生物学后果、耐受机制以及它们如何在双链和单链 DNA 中修复。