T 4 -mediated v-gene reactivation of UV-irradiated phage Ti, and its comparison with host-cell reactivation
Harm, W.
Mutation Research 17(2): 163-176
1973
ISSN/ISBN: 0027-5107 PMID: 4684400 Document Number: 62211
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 Bs−1, or K12 strains carrying a uvr A or uvr C 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 T4ν1 is used for superinfection, and is therefore called ν-gene reactivation (v R) of T1. Comparison of Hcr and v R shows that maximal Hcr of T1 is usually observed in only a minor fraction of the host-cell population, while maximal v R of T1 occurs in most, if not all, of the v R-proficient complexes. Caffeine at a permanent concentration of 2 mg/ml, or acriflavine at 3 μg/ml, inhibits Hcr completely but effects v R of T1 little or not at all. Preirradiation of the host cells inhibits Hcr considerably more than v R of T1, and does not affect v R of T4. v R 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.