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E. coli cells lysogenic for the thermoinducible prophage XcI857 can be transiently induced by a brief heat treatment. Although this treatment does not kill the cells, some X 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 recBstrain, which is normally much more radiosensitive than its recB+ parent. After pulse-heating at 420, the survival curve of E. coli recB-lysogenized with XcI857 does not differ from that of the wild-type strain. Since X red mutants do not increase the radioresistance of recB-strains, both X red gene products, X exonuclease and dl-protein, are required to compensate for the missing recB product.Furthermore, phage-induced radioresistance also occurs in recB+ lysogens even when they carry X red-, but not when the X 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 -y-protein.

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