Keweloh H, Bakker E P
J Bacteriol. 1984 Oct;160(1):347-53. doi: 10.1128/jb.160.1.347-353.1984.
The nature of the bacteriophage T1-induced changes in the permeability of the cytoplasmic membrane of Escherichia coli K-12 was investigated. At 20 degrees C and with glucose as a substrate, the addition of one bacteriophage per cell induced a complete and irreversible loss of K+ ions (single-hit phenomenon). K+ loss was compensated by an uptake of Na+, Li+, or choline by the cell, depending on which of these ions was the major cation in the medium. T1 depolarized the cells and inhibited 86Rb+-K+ exchange across the cytoplasmic membrane. The loss of K+ occurred independently of the Mg2+ concentration in the medium. By contrast, at low but not at high Mg2+ concentrations, T1 caused efflux of Mg2+ which in turn caused inhibition of respiration and a decrease of delta pH.
研究了噬菌体T1诱导的大肠杆菌K - 12细胞质膜通透性变化的性质。在20摄氏度且以葡萄糖为底物的条件下,每个细胞添加一个噬菌体可诱导K⁺离子完全且不可逆的损失(单打击现象)。细胞通过摄取Na⁺、Li⁺或胆碱来补偿K⁺的损失,这取决于这些离子中哪一种是培养基中的主要阳离子。T1使细胞去极化,并抑制细胞质膜上的⁸⁶Rb⁺ - K⁺交换。K⁺的损失与培养基中Mg²⁺的浓度无关。相比之下,在低Mg²⁺浓度而非高Mg²⁺浓度下,T1导致Mg²⁺外流,进而导致呼吸抑制和ΔpH降低。