Enlargement of Escherichia coli after bacteriophage infection. I. Description of the phenomenon.
Escherichia coli B/r and B(s-1) ceased division and increased in mean cell volume soon after infection with T-even phage. The effect was obtained with wild-type or rapid lysis mutants, as well as with ultraviolet light-killed phage and with bacteriophage ghosts which lack deoxyribonucleic acid. The cell response did not require the presence of phage genetic material or the production of progeny phage. A Poisson distribution of the fraction of adsorbed phage at different multiplicites of infection indicates that one phage per bacterium will produce maximum increase in cell volume. T-even phage-resistant E. coli mutants showed no enlargement response, and phage T1, T3, and T7 elicited neither abrupt termination of cell division nor host cell enlargement. Infection with baseplate-defective T4D 12(-) amber mutants, which bind reversibly to but do not penetrate the bacterium, also had no effect. In vitro restoration of normal baseplate function in these defective viruses allowed phage adsorption and penetration and caused host cell division arrest and enlargement. These findings indicate that arrest of division and increase in mean cell volume occur together when a sensitive strain of E. coli is infected with T-even phage that adsorb and penetrate normally.
D001431:Bacteriological Techniques; D002455:Cell Division; D002474:Cell-Free System; D003090:Coliphages / Q000254:growth & development* / Q000528:radiation effects; D004926:Escherichia coli / Q000166:cytology*; D005827:Genetics, Microbial; D008242:Lysogeny; D008854:Microscopy, Electron; D009154:Mutation; D011830:Radiation Effects; D013997:Time Factors; D014466:Ultraviolet Rays