Nucleotide excision repair (NER) is a DNA repair pathway present in all domains of life. In bacteria, UvrA protein localizes the DNA lesion, followed by verification by UvrB helicase and excision by UvrC double nuclease. UvrA senses deformations and flexibility of the DNA duplex without precisely localizing the lesion in the damaged strand, an element essential for proper NER. Using a combination of techniques, we elucidate the mechanism of the damage verification step in bacterial NER. UvrA dimer recruits two UvrB molecules to its two sides. Each of the two UvrB molecules clamps a different DNA strand using its β-hairpin element. Both UvrB molecules then translocate to the lesion, and UvrA dissociates. The UvrB molecule that clamps the damaged strand gets stalled at the lesion to recruit UvrC. This mechanism allows UvrB to verify the DNA damage and identify its precise location triggering subsequent steps in the NER pathway.

中文翻译：

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结合结构和生化方法揭示了 UvrB 在 DNA 病变上的易位和停滞作为细菌核苷酸切除修复中损伤验证的机制。

核苷酸切除修复 (NER) 是一种存在于所有生命领域的 DNA 修复途径。在细菌中，UvrA 蛋白定位 DNA 损伤，然后通过 UvrB 解旋酶验证并通过 UvrC 双核酸酶切除。UvrA 可以感知 DNA 双链体的变形和柔韧性，而无需精确定位受损链中的病变，这是正确 NER 必不可少的元素。使用多种技术，我们阐明了细菌 NER 中损伤验证步骤的机制。UvrA 二聚体在其两侧招募两个 UvrB 分子。两个 UvrB 分子中的每一个都使用其 β-发夹元件夹住不同的 DNA 链。然后两个 UvrB 分子都转移到病灶，UvrA 解离。夹住受损链的 UvrB 分子在病变处停滞以招募 UvrC。