HOST-CELL REACTIVATION OF NON-LETHAL ULTRAVIOLET-EFFECTS

Abstract— Delay of intracellular growth of u.v.-irradiated bacteriophage T1 and Λ was compared in host-cell reactivating HCR(+)] and non-host-cell reactivating HCR(—)] bacterial strains. At a given phage survival level, intracellular growth delay occurs to the same extent in HCR (+) and HCR (-) strains; at a given absolute u.v.-dose, this delay is considerably more expressed in HCR (-) than in HCR (+) strains. Therefore, it does not reflect the time required for the HCR repair of otherwise lethal U.V. lesions. The results rather suggest that U.V. causes, besides lethal lesions, stable photoproducts in the DNA, which are a priori non-lethal, and which are recognized and efficiently eliminated by the HCR repair system. The HCR enzymes likewise act on (non-lethal) u.v.-photoproducts causing prophage induction in lysogenic cells. Consequently, one obtains the maximum induction effect in a lysogenic HCR (-) strain at a much lower u.v.-dose than in the corresponding lysogenic HCR (+) strain. In contrast, u.v.-damage causing loss of the host cell's capacity to support growth of unirradiated phage is not affected by HCR.