Physiological and Genetic Aspects of Abortive Infection of a Shigella sonnei Strain by Coliphage T7

Abstract

Phage T7 adsorbed to and lysed cells of Shigella sonnei D 2 371-48, although the average burst size was only 0.1 phage per cell (abortive infection). No mechanism of host-controlled modification was involved. Upon infection, T7 rapidly degraded host deoxyribonucleic acid (DNA) to acid-soluble material. Phage-directed DNA synthesis was initiated normally, but after a few minutes the pool of phage DNA, including the parental DNA, was degraded. Addition of chloramphenicol, at the time of phage infection, prevented both the initiation of phage-directed DNA synthesis and the degradation of parental phage DNA. Addition of chloramphenicol 4.5 min after phage was added permitted the onset of phage-directed DNA synthesis but prevented breakdown of phage DNA. Mutants of T7 ( ss − mutants) have been isolated which show normal growth in strain D 2 371-48. Upon mixed infection of this strain with T7 wild type and an ss − mutant, infection was abortive; no complementation occurred. The DNA of the ss − mutants was degraded in mixed infection like that of the wild type. Revertant mutants which have lost their ability to grow on D 2 371-48 were isolated from ss − mutants; they are, in essence, phenotypically like T7 wild type. Independently isolated revertants of ss − mutants did not produce ss − recombinants when they were crossed among themselves. When independently isolated ss − mutants were crossed with each other, wild-type recombinants were found; ss − mutants could then be mapped in a cluster compatible with the length of one cistron. We concluded that T7 codes for an active, chloramphenicol-sensitive function [ ss + function (for suicide in Shigella )] which leads to the breakdown of phage DNA in the Shigella host.