Wang T C, Smith K C
J Bacteriol. 1986 Nov;168(2):940-6. doi: 10.1128/jb.168.2.940-946.1986.
The mechanism by which recA (Srf) mutations (recA2020 and recA801) suppress the deficiency in postreplication repair shown by recF mutants of Escherichia coli was studied in UV-irradiated uvrB and uvrA recB recC sbcB cells. The recA (Srf) mutations partially suppressed the UV radiation sensitivity of uvrB recF, uvrB recF recB, and uvrA recB recC sbcB recF cells, and they partially restored the ability of uvrB recF and uvrA recB recC sbcB recF cells to repair DNA daughter-strand gaps. In addition, the recA (Srf) mutations suppressed the recF deficiency in the repair of DNA double-strand breaks in UV-irradiated uvrA recB recC sbcB recF cells. The recA2020 and recA801 mutations do not appear to affect the synthesis of UV radiation-induced proteins, nor do they appear to produce an altered RecA protein, as detected by two-dimensional gel electrophoresis. These results are consistent with the suggestion (M. R. Volkert and M. A. Hartke, J. Bacteriol. 157:498-506, 1984) that the recA (Srf) mutations do not act by affecting the induction of SOS responses; rather, they allow the RecA protein to participate in the recF-dependent postreplication repair processes without the need of the RecF protein.
在紫外线照射的uvrB和uvrA recB recC sbcB细胞中，研究了recA（Srf）突变（recA2020和recA801）抑制大肠杆菌recF突变体所表现出的复制后修复缺陷的机制。recA（Srf）突变部分抑制了uvrB recF、uvrB recF recB和uvrA recB recC sbcB recF细胞对紫外线辐射的敏感性，并部分恢复了uvrB recF和uvrA recB recC sbcB recF细胞修复DNA子链缺口的能力。此外，recA（Srf）突变抑制了uvrA recB recC sbcB recF细胞在紫外线照射后修复DNA双链断裂时的recF缺陷。recA2020和recA801突变似乎不影响紫外线辐射诱导蛋白的合成，二维凝胶电泳检测也未发现它们产生改变的RecA蛋白。这些结果与以下观点一致（M. R. Volkert和M. A. Hartke，《细菌学杂志》157:498 - 506，1984），即recA（Srf）突变不是通过影响SOS反应的诱导起作用；相反，它们使RecA蛋白能够在不需要RecF蛋白的情况下参与依赖recF的复制后修复过程。
