Freedman M L, Krisch R E
J Virol. 1971 Jul;8(1):87-94. doi: 10.1128/JVI.8.1.87-94.1971.
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.
用T偶数噬菌体感染大肠杆菌B/r和B(s - 1)后不久,它们就停止分裂,平均细胞体积增大。野生型或速溶突变体、紫外线灭活的噬菌体以及缺乏脱氧核糖核酸的噬菌体空壳都能产生这种效应。细胞反应不需要噬菌体遗传物质的存在或子代噬菌体的产生。在不同感染复数下吸附噬菌体的比例呈泊松分布,这表明每个细菌一个噬菌体将使细胞体积增加到最大。抗T偶数噬菌体的大肠杆菌突变体没有表现出体积增大的反应,噬菌体T1、T3和T7既没有引起细胞分裂的突然终止,也没有导致宿主细胞增大。用基板缺陷型T4D 12(-)琥珀突变体感染,该突变体与细菌可逆结合但不穿透细菌,也没有效果。在这些缺陷病毒中体外恢复正常基板功能可使噬菌体吸附和穿透,并导致宿主细胞分裂停止和体积增大。这些发现表明,当正常吸附和穿透的T偶数噬菌体感染敏感的大肠杆菌菌株时,分裂停止和平均细胞体积增加会同时发生。