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When Escherichia coli cells are gamma irradiated they degrade their deoxyribonucleic acid (DNA). The DNA of previously gamma-irradiated T4 phage is also degraded in infected cells. The amount of degradation is not only dependent on the dose but also on the genotype of the cell. The amount of degradation is less in cells carrying a recB or a recC mutation, suggesting that most of the DNA degradation is due to the recB(+) and recC(+) gene product (exonuclease V). In some strains a previous dose of ultraviolet (UV) light followed by incubation renders the cells resistant to DNA degradation after gamma irradiation. We have shown this inhibition to take place for infecting T4 phage also. By using six strains of E. coli selected for mutations in the genes recA, exr (or lex), and uvrB, we have been able to show that the preliminary UV treatment produces no change in recA and exr cells for both endogenous DNA degradation and the degradation of infecting irradiated T4 phage DNA, i.e., inhibition was not detected in these strains. On the other hand, wild-type cells and strains carrying mutations of uvrB show inhibition in both types of experiments. Because the recA gene product and the exr(+) (lex(+)) gene product are necessary for the induction of prophage, it is possible that the phenomenon of inducible inhibition requires recA(+) and exr(+) presence. One interpretation of these results is that an inducible inhibitor may be controlled by the exr gene.

The loss in capacity of irradiated bacteria to support the growth of T4 phage has been studied for two strains, Escherichia coli B and E. coli B(s-1). Following a dose of 25 krads, the capacity is quite rapidly lost during postirradiation incubation so that after two hr of such incubation at 37 C only 12% remains in strain B and 3% in strain B(s-1). Evidence that capacity is lost in an all-or-none fashion was provided by two types of experiments: (i) a single-burst analysis of those cells which survived to give a burst, and (ii) an analysis of the regulation of an early phage enzyme. Several processes were examined to try to determine the cause of the loss in capacity. These were the ability of the irradiated and postirradiation incubated cells to respire, to allow phage adsorption and injection of phage deoxyribonucleic acid, to support the transcription and translation of an early gene, and to support replication of phage deoxyribonucleic acid. Of these processes, transcription and translation appeared to be the most closely associated with the capacity loss, although respiration was reduced to 50% after 2 hr.