DNA double-strand breaks (DSBs) are a hazardous form of damage that can potentially cause cell death or genomic rearrangements. In mammalian G1- and G2-phase cells, DSBs are repaired with two-component kinetics. In both phases, a fast process uses canonical nonhomologous end joining (c-NHEJ) to repair the majority of DSBs. In G2, slow repair occurs by homologous recombination. The slow repair process in G1 also involves c-NHEJ proteins but additionally requires the nuclease Artemis and DNA end resection. Here, we consider the nature of slow DSB repair in G1 and evaluate factors determining whether DSBs are repaired with fast or slow kinetics. We consider limitations in our current knowledge and present a speculative model for Artemis-dependent c-NHEJ and the environment underlying its usage.

DNA 双链断裂 (DSB) 是一种危险的损伤形式，可能导致细胞死亡或基因组重排。在哺乳动物 G1 期和 G2 期细胞中，DSB 用双组分动力学进行修复。在这两个阶段中，快速过程使用规范的非同源末端连接 (c-NHEJ) 来修复大多数 DSB。在 G2 中，通过同源重组进行缓慢修复。G1 期的缓慢修复过程也涉及 c-NHEJ 蛋白，但还需要核酸酶 Artemis 和 DNA 末端切除。在这里，我们考虑 G1 中慢速 DSB 修复的性质，并评估决定 DSB 是否以快速或慢速动力学修复的因素。我们考虑了我们当前知识的局限性，并提出了依赖于 Artemis 的 c-NHEJ 及其使用环境的推测模型。