质粒R391的紫外线致敏功能干扰了大肠杆菌复制后修复的后期步骤。

The ultraviolet-sensitizing function of plasmid R391 interferes with a late step of postreplication repair in Escherichia coli.

作者信息

Wang T C, de Saint Phalle B, Millman K L, Fowler R G

机构信息

Department of Molecular Biology, Chang Gung College of Medicine and Technology, Kwei-San, Tao-Yuan, Taiwan.

出版信息

Mutat Res. 1996 Apr 2;362(3):219-26. doi: 10.1016/0921-8777(95)00044-5.

DOI:10.1016/0921-8777(95)00044-5

PMID:8637500

Abstract

The conjugative plasmid R391 increases the UV radiation sensitivity of wild-type, uvrA, and lexA cells of Escherichia coli, but not recA strains. To investigate the UV-sensitizing function of R391, we examined the effect of R391 on the repair of DNA daughter-strand gaps and on the UV radiation sensitivities of various repair and/or recombination-deficient mutants. The presence of R391 did not significantly inhibit the repair of DNA daughter-strand gaps in uvrB cells. The presence of R391 increased the UV radiation sensitivity of uvrA, uvrA recF, uvrB, uvrB recF, uvrB recB, and uvrB ssb-113 cells to UV irradiation, but did not significantly increase the UV radiation sensitivity of uvrA ruvA and uvrA ruvC strains. Based on these results, we propose that the UV-sensitizing activity of R391 acts by inhibiting or interfering with the ruvABC-mediated postsynapsis step of recombinational repair.

摘要

接合质粒R391可增加大肠杆菌野生型、uvrA和lexA细胞对紫外线辐射的敏感性，但不会增加recA菌株的敏感性。为了研究R391的紫外线致敏功能，我们检测了R391对DNA子链缺口修复的影响以及对各种修复和/或重组缺陷型突变体紫外线辐射敏感性的影响。R391的存在并未显著抑制uvrB细胞中DNA子链缺口的修复。R391的存在增加了uvrA、uvrA recF、uvrB、uvrB recF、uvrB recB和uvrB ssb-113细胞对紫外线照射的敏感性，但并未显著增加uvrA ruvA和uvrA ruvC菌株的紫外线辐射敏感性。基于这些结果，我们提出R391的紫外线致敏活性是通过抑制或干扰ruvABC介导的重组修复的突触后步骤来发挥作用的。