因暴露于紫外线而受损的碱基干扰转录，造成RNA聚合酶停滞。UvrD（核苷酸切除修复所需的一种DNA螺旋酶）能清除这种病灶，但其精确作用过去并不清楚。现在，Evgeny Nudler及同事发现，UvrD是一个转录伸长因子，结合RNA聚合酶，并当后者在一个病灶处停滞下来时促进其向后运动。NusA （另一个伸长因子）辅助促进原路返回运动，帮助UvrD将其他核苷酸切除修复因子定向到所暴露的病灶。
UvrD helicase is required for nucleotide excision repair, although its role in this process is not well defined. Here we show that Escherichia coli UvrD binds RNA polymerase during transcription elongation and, using its helicase/translocase activity, forces RNA polymerase to slide backward along DNA. By inducing backtracking, UvrD exposes DNA lesions shielded by blocked RNA polymerase, allowing nucleotide excision repair enzymes to gain access to sites of damage. Our results establish UvrD as a bona fide transcription elongation factor that contributes to genomic integrity by resolving conflicts between transcription and DNA repair complexes. Furthermore, we show that the elongation factor NusA cooperates with UvrD in coupling transcription to DNA repair by promoting backtracking and recruiting nucleotide excision repair enzymes to exposed lesions. Because backtracking is a shared feature of all cellular RNA polymerases, we propose that this mechanism enables RNA polymerases to function as global DNA damage scanners in bacteria and eukaryotes.