Wagner E F, Ponta H, Schweiger M
J Biol Chem. 1980 Jan 25;255(2):534-9.
In the interaction between Escherichia coli virus T1 and its host cell, which leads to reorientation of macromolecule synthesis, the alteration of the host cell membrane is an important step: The proton-motive force is rapidly reduced. This became apparent from selective changes in energy-coupled transports: proton-motive force- and ATP-dependent transports are inhibited in wild type cells. However, in ATPase-deficient (unc-) cells the ATP-driven transports are not affected by T1. The membrane potential is reduced by T1 as was measured by triphenylmethylphosphonium ion distribution. The potassium gradient is dissipated and calcium ions are accumulated by the cells. However, the residual (but reduced) membrane energy is essential for T1 development since the addition of uncouplers prevents any viral production. Consistently, the cell membrane remains intact after T1 infection: proteins, like beta-galactoside, amino acids, and alpha-methylglucoside cannot passively penetrate the membrane of T1-infected cells.
在大肠杆菌病毒T1与其宿主细胞的相互作用中,这种相互作用会导致大分子合成重新定向,宿主细胞膜的改变是一个重要步骤:质子动力迅速降低。这从能量偶联转运的选择性变化中明显看出:野生型细胞中质子动力和ATP依赖性转运受到抑制。然而,在ATP酶缺陷(unc-)细胞中,ATP驱动的转运不受T1影响。通过三苯甲基鏻离子分布测量发现,T1可降低膜电位。细胞的钾梯度消散,钙离子积累。然而,残余(但已降低)的膜能量对于T1的发育至关重要,因为添加解偶联剂会阻止任何病毒产生。一致的是,T1感染后细胞膜保持完整:蛋白质,如β-半乳糖苷、氨基酸和α-甲基葡萄糖苷不能被动穿透T1感染细胞的膜。