Host influence on the activity of genes c1 and c3 in regulating the decision between lysis and lysogency in bacteriophage P22.

A Polymyxin B-sensitive mutant of Salmonella typhimurium (Pox-1) channels all infecting wild-type P22 toward lysogenization. The efficiency of this channeling is sufficiently high that P22c+ (wild type) cannot form plaques on Pox-1; phage mutants defective in repressor synthesis (P22c1, c2, c3) or refractory toward repressor (P22vir B) can form plaques. The lytic growth of all phages which have a functional c1 gene is retarded in Pox-1; this retardation is seen even in phages which cannot make repressor. We present experiments which are consistent with the explanation that the retardation is an exaggeration of a normal regulatory event. In a wild-type host, P22 genes c1 and c3 products, host RNA polymerase, and other host factors (?) interact at a promotor site (c27) IN THE PHAGE DNA. This interaction promotes repressor synthesis and represses transcription of lytic genes. In the mutant Pox-1, a host product involved in viral DNA synthesis and transcription is altered. The altered host product results in stronger retardation of lytic gene transcription. The importance of this interaction in the decision between lysis and lysogeny is discussed. The mutant Pox-1 alters the expression or activity of another phage gene. Gene c3 product is absolutely required for lysogenization in this host, although it is not so required in wild-type S. typhimurium.