T 4-mediated ν-gene reactivation of UV-irradiated phage T1, and its comparison with host-cell reactivation

Abstract

UV-irradiated (254 nm) phage T1 undergo host-cell reactivation (HCR) after infection of Escherichia coli cells possessing an intact excision-resynthesis repair system. The present results show that T1 can also be reactivated in host-cell reactivation defective (HCR −) bacteria ( E. coli B s−1, or K12 strains carrying a uvrA or uvrC mutation), if these are superinfected with heavily UV-irradiated phage T4. This effect, which reflects an average repair of 70% of the T1 lethal lesions, requires the ν gene function of T4. It is not observed when the mutant T4 ν 1 is used for superinfection, and is therefore called ν-gene reactivation (vR) of T1. Comparison of HCR and vR shows that maximal HCR of T1 is usually observed in only a minor fraction of the host-cell population, while maximal vR of T1 occurs in most, if not all, of the vR-proficient complexes. Caffeine at a permanent concentration of 2 mg/ml, or acriflavine at 3 μg/ml, inhibits HCR completely but effects vR of T1 little or not at all. Preirradiation of the host cells inhibits HCR considerably more than vR of T1, and does not affect vR of T4. vR occurs also in HCR + host cells, where it increases the T1 survival only slightly. Presumably the bacterial UV endonuclease involved in HCR, and lacking in HCR − cells, can be replaced by the T4 UV endonuclease to permit excision repair in T1, but it seems likely that the enzymes engaged in later repair steps are of bacterial rather than T4 origin.