Phenotypic delay of expression of UV-induced c mutations in prophage kappa

Abstract

UV irradiation of stationary kappa lysogenic cells of Serratia marcesens HY leads to a frequency of up to 35% c mutants after several hours of post-irradiation incubation. Dose and time curves of titers of wild-type and c-mutant phages as well as single bursts were studied. The curves show that the high c frequency was not due to an unusually high mutation rate but to ( 1) a low frequency of UV induction of phage development (<10 −3) and ( 2) a very high probability of burst of non-induced cells containing a c-mutated prophage. Phenotypic expression of a UV-induced c mutation in the prophage was delayed for several cell divisions until the c prophage developed lytically because it cannot be kept repressed. Because of such cell multiplication the size of a c clone was several times the normal burst size after a few hours of incubation. Nearly all induced c mutations belong to the c 111 region of the phage genome, this region being responsible for keeping the prophage repressed. It is assumed that active prophage repressor (p-repressor) is no longer produced after a c mutation of the prophage has occurred, and hence that it disappears during the next few cell divisions leading to bursts that liberate c mutants. Investigations of colonies grown from survivors of infections with free wild or c 111-type phages indicate that after infection a gene product (i-repressor) is formed with the same chance by c 111 as by the wild type. This product represses lytic development and thus causes cells to survive superinfection until a stable lysogeny (by wild type) or an “unstable lysogeny” (by c 111 mutants) is established.