On the darkreactivation mechanism in ultraviolet irradiated bacteria

Abstract

The decrease in the rate of photoreactivation (PhR) of ultraviolet (u.v.) irradiated phage due to u.v. irradiation of bacteria ( Lennox et al. 1954) is understood as a competing effect of the u.v. lesions in the bacterial nucleic acids for the PhR enzyme ( Metzger 1963). This competing effect is neutralized either by darkreactivation (DR) or by PhR of the bacteria before phage infection. The occurrence of DR is restricted to bacteria which can perform hostcell-reactivation (HCR) on u.v. irradiated phage Tl. For HCR of phage Tl, Sauerbier (1961, 1962a, 1962b) has proposed an enzymatic repair mechanism. The strictly linked occurrence of HCR and DR suggests that the two phenomena are based on the same mechanism. The experiments described in this paper demonstrate: 1) HCR and DR are achieved by the same enzyme. 2) DR directly repairs the u.v. lesions. 3) PhR and DR repair the same lesions in nucleic acids. 4) The enzyme is neither induced by phage infection nor by u.v. irradiation, but is normally present in the bacterial cell. 5) The action of the enzyme is inhibited by caffeine.