DNA repair is essential for cell survival. In all domains of life, error-prone and error-free repair pathways ensure maintenance of genome integrity under stress. Although mutagenic, low fidelity repair mechanisms help avoid potential lethality associated with unrepaired damage, thus making them important for genome maintenance, and in some cases, the preferred mode of repair. However, cells carefully regulate pathway choice to restrict activity of these pathways to only certain conditions. One such repair mechanism is Translesion Synthesis (TLS), where a low fidelity DNA polymerase is employed to synthesize across a lesion. In bacteria, TLS is a potent source of stress-induced mutagenesis, with potential implications in cellular adaptation as well as antibiotic resistance. Extensive genetic and biochemical studies, predominantly in Escherichia coli, have established a central role for TLS in bypassing bulky DNA lesions associated with ongoing replication, either at or behind the replication fork. More recently, imaging-based approaches have been applied to understand the molecular mechanisms of TLS and how its function is regulated. Together, these studies have highlighted replication-independent roles for TLS as well. In this review, we discuss the current status of research on bacterial TLS, with emphasis on recent insights gained mostly through microscopy at the single-cell and single-molecule level.

中文翻译：

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可视化诱变修复：对细菌跨损伤合成的新见解。

DNA 修复对于细胞生存至关重要。在生命的各个领域，容易出错和无错的修复途径可确保在压力下维持基因组完整性。尽管具有诱变性，但低保真度修复机制有助于避免与未修复的损伤相关的潜在致命性，从而使它们对于基因组维护很重要，并且在某些情况下是首选的修复模式。然而，细胞仔细调节通路选择，将这些通路的活性限制在某些条件下。其中一种修复机制是跨损伤合成 (TLS)，其中采用低保真度 DNA 聚合酶跨损伤进行合成。在细菌中，TLS 是应激诱导突变的有效来源，对细胞适应和抗生素耐药性具有潜在影响。广泛的遗传和生化研究（主要是在大肠杆菌中）已经确定了 TLS 在绕过复制叉处或复制叉后与持续复制相关的大量 DNA 损伤方面发挥的核心作用。最近，基于成像的方法已被应用于了解 TLS 的分子机制及其功能如何调节。总之，这些研究也强调了 TLS 的复制独立作用。在这篇综述中，我们讨论了细菌 TLS 的研究现状，重点是最近主要通过单细胞和单分子水平的显微镜获得的见解。