Hagensee M E, Moses R E
J Bacteriol. 1986 Dec;168(3):1059-65. doi: 10.1128/jb.168.3.1059-1065.1986.
The repair response of Escherichia coli to hydrogen peroxide-induced DNA damage was investigated in intact and toluene-treated cells. Cellular DNA was cleaved after treatment by hydrogen peroxide as analyzed by alkaline sucrose sedimentation. The incision step did not require ATP or magnesium and was not inhibited by N-ethylmaleimide (NEM). An ATP-independent, magnesium-dependent incorporation of nucleotides was seen after the exposure of cells to hydrogen peroxide. This DNA repair synthesis was not inhibited by the addition of NEM or dithiothreitol. In dnaB(Ts) strain CRT266, which is thermolabile for DNA replication, normal levels of DNA synthesis were found at the restrictive temperature (43 degrees C), showing that DNA replication was not necessary for this DNA synthesis. Density gradient analysis also indicated that hydrogen peroxide inhibited DNA replication and stimulated repair synthesis. The subsequent reformation step required magnesium, did not require ATP, and was not inhibited by NEM, in agreement with the synthesis requirements. This suggests that DNA polymerase I was involved in the repair step. Furthermore, a strain defective in DNA polymerase I was unable to reform its DNA after peroxide treatment. Chemical cleavage of the DNA was shown by incision of supercoiled DNA with hydrogen peroxide in the presence of a low concentration of ferric chloride. These findings suggest that hydrogen peroxide directly incises DNA, causing damage which is repaired by an incision repair pathway that requires DNA polymerase I.
在完整细胞和经甲苯处理的细胞中研究了大肠杆菌对过氧化氢诱导的DNA损伤的修复反应。用过氧化氢处理后,通过碱性蔗糖沉降分析发现细胞DNA被切割。切口步骤不需要ATP或镁,也不受N-乙基马来酰亚胺(NEM)抑制。细胞暴露于过氧化氢后,观察到核苷酸的ATP非依赖性、镁依赖性掺入。添加NEM或二硫苏糖醇不会抑制这种DNA修复合成。在对DNA复制不耐热的dnaB(Ts)菌株CRT266中,在限制温度(43摄氏度)下发现了正常水平的DNA合成,表明这种DNA合成不需要DNA复制。密度梯度分析还表明,过氧化氢抑制DNA复制并刺激修复合成。随后的重新形成步骤需要镁,不需要ATP,也不受NEM抑制,这与合成要求一致。这表明DNA聚合酶I参与了修复步骤。此外,DNA聚合酶I缺陷的菌株在过氧化物处理后无法重新形成其DNA。在低浓度氯化铁存在下用过氧化氢切割超螺旋DNA表明了DNA的化学切割。这些发现表明,过氧化氢直接切割DNA,造成损伤,损伤通过需要DNA聚合酶I的切口修复途径进行修复。