Ionizing Radiation-induced Lesions in T4 Phage andEscherichia ColiDNAs as Sites for Initiation of Degradationin Vivo

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Abstract
The preceding paper showed that the radiation-induced T4 DNA degradation which occurs when gamma-irradiated T4 phage infect E. coli is initiated at ionizing radiation lesions in the DNA. We extend the results here to show that the endogenous cellular DNA degradation which follows gamma-irradiation of E. coli is also initiated at ionizing-radiation lesions in the DNA itself. This result was obtained by comparing the patterns of DNA degradation of gamma-irradiated T4 DNA in various radiation-sensitive Escherichia coli strains with the reported patterns of gamma-ray-induced endogenous bacterial DNA degradation in the same corresponding strains. There were the following similarities: (1) recBC nuclease (recB and recC genes) that is responsible for DNA degradation of irradiated E. coli cells is also responsible for the degradation of DNA of the irradiated T4 phage. (2) An increased degradation of both DNAs is seen in polA1− cells over that in the parental polA1+ cells. (3) The enzymatic defect in uvr− strains A, B or C all show the same lack of effect on the levels of degradation of phage DNA as that shown for bacterial DNA degradation, the levels being the same as in their parental uvr+ strain. (4) The main products of the degradation of these DNAs, followed by 3H-thymidine labelling, are thymine and a phosphorylated derivative of thymidine. The slope of the plaque-forming survival curve of gamma-irradiated T4 on P3478 and JG138 (polA1−) is 10 per cent greater than that on W3110 and JG139 (pol+). Endonuclease I defect has no effect on the level of degradation of DNA of gamma-irradiated T4 seen in endonuclease I+ parental strain.