It is well established that DNA double-strand break (DSB) repair is required to underpin chromosomal DNA replication. Because DNA replication forks are prone to breakage, faithful DSB repair and correct replication fork restart are critically important. Cells, where the proteins required for DSB repair are absent or altered, display characteristic disturbances to genome replication. In this review, we analyze how bacterial DNA replication is perturbed in DSB repair mutant strains and explore the consequences of these perturbations for bacterial chromosome segregation and cell viability. Importantly, we look at how DNA replication and DSB repair processes are implicated in the striking recent observations of DNA amplification and DNA loss in the chromosome terminus of various mutant Escherichia coli strains. We also address the mutant conditions required for the remarkable ability to copy the entire E. coli genome, and to maintain cell viability, even in the absence of replication initiation from oriC, the unique origin of DNA replication in wild type cells. Furthermore, we discuss the models that have been proposed to explain these phenomena and assess how these models fit with the observed data, provide new insights and enhance our understanding of chromosomal replication and termination in bacteria.

中文翻译：

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细菌 DNA 双链断裂修复蛋白在染色体 DNA 复制中的作用。

众所周知，DNA 双链断裂 (DSB) 修复是支持染色体 DNA 复制所必需的。由于 DNA 复制叉容易断裂，因此忠实的 DSB 修复和正确的复制叉重启至关重要。DSB 修复所需的蛋白质缺失或改变的细胞会表现出基因组复制的特征性干扰。在这篇综述中，我们分析了 DSB 修复突变株中细菌 DNA 复制如何受到干扰，并探讨了这些干扰对细菌染色体分离和细胞活力的影响。重要的是，我们研究了 DNA 复制和 DSB 修复过程如何与最近观察到的各种突变大肠杆菌菌株染色体末端的 DNA 扩增和 DNA 丢失有关。我们还解决了复制整个大肠杆菌基因组的卓越能力所需的突变条件，并维持细胞活力，即使在没有来自oriC（野生型细胞中 DNA 复制的独特起点）的复制起始的情况下。此外，我们讨论了为解释这些现象而提出的模型，并评估这些模型如何与观察到的数据相吻合，提供新的见解并增强我们对细菌中染色体复制和终止的理解。