Abstract
Wild-type Escherichia coli and a thermosensitive cell division (snake-forming) mutant were examined for killing and inhibition of protein synthesis by ghosts of bacteriophage T4. Although in both hosts these ghost-mediated effects followed single-hit kinetics, the probability of killing by a single ghost particle was greatly reduced in the much longer divisionless cells. In contrast, the inhibition of protein synthesis was similar in both hosts. Ghosts act also on DNA-less minicells as evidenced by the inhibition of leucine uptake after ghost infection. Preinfection of E. coli with wild-type T4 renders the host cell immune to the effects of superinfecting ghosts. This immunity against ghosts is dependent upon protein synthesis and, under optimal conditions, becomes complete after 2.5–3 min. Evidence is presented suggesting that the immunity reaction does not follow one-hit kinetics in the divisionless mutant. A rapid method has been developed for screening mutants of T4 for the inability to to protect host cells against superinfecting ghosts. Various mutants were tested representing genes rII, 1, 30, 39, 41, 45, 46, 47, 52, 56, 58–61, 59, and 60. A single mutant of gene 39, amE142(39) was found to differ from all the others, including 21 mutants of the same gene, in that it failed to provide immunity.
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