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WhenEscherichia 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 arecB or arecC mutation, suggesting that most of the DNA degradation is due to therecB + andrecC + 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 ofE. coli selected for mutations in the genesrecA, exr (orlex ), anduvrB , we have been able to show that the preliminary UV treatment produces no change inrecA andexr 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 ofuvrB show inhibition in both types of experiments. Because therecA gene product and theexr + (lex + ) gene product are necessary for the induction of prophage, it is possible that the phenomenon of inducible inhibition requiresrecA + andexr + presence. One interpretation of these results is that an inducible inhibitor may be controlled by theexr gene.

Involvement of recA and exr Genes in the In Vivo Inhibition of the recBC Nuclease