The Mechanisms of Lambda Virulence II. Regulatory Mutations in Classical Virulence

Abstract

Bacteria carrying λ prophage are immune to superinfection by homoimmune phage because they produce the λ repressor. The repressor controls λ gene expression and λ DNA replication through its interaction at two operators within the immunity region (Kaiser and Jacob, 1957; Isaacs, Echols, and Sly, 1965; Ptashne and Hopkins, 1968). Lambda mutants which can overcome repression and productively infect an immune host on single infection are called virulent. At least two types of virulent mutants are known, the λc17cI type (Pereira da Silva and Jacob, 1968; Packman and Sly. 1968) and the λvir described by Jacob and Wollman (1954), often referred to as classical λvir.

Earlier results (Packman and Sly, 1968; Sly and Rabideau, 1969) suggested that mutation to virulence results from two new properties of virulent mutants, constitutive replication of phage DNA and turn-on of gene N. The virulence of λc17cI was explained by the new-promoter mutation, c17 (Roberts, 1970) conferring constitutive DNA replication, and the cI mutation which permits the replicating DNA to oversaturate the repressor produced by the prophage.

This report concerns the virulence of λvir. Although initially thought to contain four mutations, Ptashne and Hopkins (1968) found only three mutations, v2 and v1v3, essential to virulence. In this paper we analyze the roles of v2 and the v1v3 combination in λvir. Although v1v3 are commonly written in this order, as in this paper, their order is not yet known. The individual effects of v1 and v3 are described in a separate report (Sly and Rabideau, submitted...