The effects of polyamines on the replication of T4 rII mutants in Escherichia coli K12 (λ)

Abstract

While rII mutants of bacteriophage T4 can replicate in Escherichia coli K12S, replication is blocked when this host is lysogenized by λ phage. Polyamines, Mg ++, and streptomycin increase the yield of rII deletion mutants in K12(λ) to varying degrees below the normal yield obtained with wild-type phage. Of a homologous series of diamines, 1,7-diaminoheptane is about 7 times more effective than 1,4-dia-aminobutane (putrescine) or Mg ++. The critical portion of the latent period for diamine stimulation is between 10 and 20 minutes after infection. In the absence of diamine, UV induction of λ replication permits subsequent rII replication; further stimulation by 1,7-diaminoheptane still occurs under these conditions. Diamines and Mg ++, unlike UV irradiation, do not bring about induction of λ phage. Uninfected cells of K12(λ) and K12S were found to contain nearly identical amounts of putrescine. Several independent methods were used to examine permeability differences between the two types of infected cells; in all cases, no significant differences in permeability to large or small molecules were found. Therefore, the inability of rII mutants to replicate in K12(λ) cannot be attributed to generalized leakage resulting from phage infection. Several alternatives are suggested for the mode of action of these substances.