Interaction of bacterial and lambda phage recombination systems in the x-ray sensitivity of Escherichia coli K-12.

E. coli cells lysogenic for the thermoinducible prophage lambdacI857 can be transiently induced by a brief heat treatment. Although this treatment does not kill the cells, some lambda products normally formed during vegetative phage development are made that can alter the response of host cells to x-irradiation by causing an increase in radioresistance. This increased resistance is particularly striking in the recombination-deficient recB-strain, which is normally much more radiosensitive than its recB(+) parent. After pulse-heating at 42 degrees , the survival curve of E. coli recB(-) lysogenized with lambdacI857 does not differ from that of the wild-type strain. Since lambda red mutants do not increase the radioresistance of recB(-) strains, both lambda red gene products, lambda exonuclease and beta-protein, are required to compensate for the missing recB product. Furthermore, phage-induced radioresistance also occurs in recB(+) lysogens even when they carry lambda red(-), but not when the lambda prophage is gam(-). Thus, in wild-type cells, phage-induced radioresistance requires some interaction between the bacterial recB gene product (exonuclease V) and the phage lambda-protein.