Wang T C, Smith K C
J Bacteriol. 1983 Dec;156(3):1093-8. doi: 10.1128/jb.156.3.1093-1098.1983.
The molecular mechanisms for the recF-dependent and recB-dependent pathways of postreplication repair were studied by sedimentation analysis of DNA from UV-irradiated Escherichia coli cells. When the ability to repair DNA daughter strand gaps was compared, uvrB recF cells showed a gross deficiency, whereas uvrB recB cells showed only a small deficiency. Nevertheless, the uvrB recF cells were able to perform some limited repair of daughter strand gaps compared with a "repairless" uvrB recA strain. The introduction of a recB mutation into the uvrB recF strain greatly increased its UV radiation sensitivity, yet decreased only slightly its ability to repair daughter strand gaps. Kinetic studies of DNA repair with alkaline and neutral sucrose gradients indicated that the accumulation of unrepaired daughter strand gaps led to the formation of low-molecular-weight DNA duplexes (i.e., DNA double-strand breaks were formed). The uvrB recF cells were able to regenerate high-molecular-weight DNA from these low-molecular-weight DNA duplexes, whereas the uvrB recF recB and uvrB recA cells were not. A model for the recB-dependent pathway of postreplication repair is presented.
通过对紫外线照射的大肠杆菌细胞的DNA进行沉降分析，研究了复制后修复的recF依赖性和recB依赖性途径的分子机制。当比较修复DNA子链缺口的能力时，uvrB recF细胞表现出严重缺陷，而uvrB recB细胞仅表现出轻微缺陷。然而，与“无修复能力的”uvrB recA菌株相比，uvrB recF细胞能够对子链缺口进行一些有限的修复。在uvrB recF菌株中引入recB突变极大地增加了其对紫外线辐射的敏感性，但仅略微降低了其修复子链缺口的能力。用碱性和中性蔗糖梯度对DNA修复进行的动力学研究表明，未修复的子链缺口的积累导致了低分子量DNA双链体的形成（即形成了DNA双链断裂）。uvrB recF细胞能够从这些低分子量DNA双链体中再生高分子量DNA，而uvrB recF recB和uvrB recA细胞则不能。本文提出了复制后修复的recB依赖性途径的模型。
