Evidence of different mechanisms for ultraviolet reactivation and “Ordinary host cell reactivation” of phage λ

Abstract

The question whether UV-reactivation (UVR) of phage λ is UV-stimulated host cell reactivation (HCR) was reexamined by methods inhibiting HCR. HCR consists of two distinct mechanisms: “Ordinary HCR” is lacking in K12 hcr − and B s-1 and is inhibited by caffeine or 5-bromouracil (5BU) substitution of λ DNA or UV irradiation of the host. A minor component, “residual HCR,” is present in K12 hcr − and B s-1, and is insensitive to caffeine and 5BU substitution of λ DNA. Even when “ordinary HCR” was blocked by simultaneously using caffeine, K12 hcr − hosts and 5BU-λ, UVR could not be abolished. We conclude, that “ordinary HCR” and UVR are achieved by (at least partially) different mechanisms of repair. Experimental evidence against the participation of nucleases in UVR was also obtained.