Tokuda H, Konisky J
Proc Natl Acad Sci U S A. 1979 Dec;76(12):6167-71. doi: 10.1073/pnas.76.12.6167.
Colicins Ia and E1 are shown to inhibit the formation and bring about the collapse of a potassium diffusion potential imposed across the membrane of liposomes prepared from soybean or Escherichia coli phospholipids. Such depolarization results from a colicin-induced increase in membrane ion permeability. Colicins E2 and E3 do not depolarize such membranes. In addition to the colicin Ia-induced rapid efflux of preloaded rubidium, sodium, phosphate, or choline from liposomes, a slower efflux of preloaded sucrose or glucose 6-phosphate occurs. However, treated liposomes do not leak inulin or dextran, demonstrating that the effects of E1 and Ia are not due to a general disruption of membrane structure. The fact that colicin-induced ion efflux is observed in the complete absence of a membrane potential shows that the action of these colicins on liposomes is not voltage dependent. These results provide strong evidence that the depolarization of E. coli cells by colicins Ia and E1 results from a colicin-induced increase in membrane permeability to ions. It is proposed that this is brought about by the direct interaction of the colicin molecules with the bacterial cytoplasmic membrane.
已表明大肠菌素Ia和E1可抑制由大豆或大肠杆菌磷脂制备的脂质体膜上施加的钾扩散电位的形成,并导致其崩溃。这种去极化是由大肠菌素诱导的膜离子通透性增加引起的。大肠菌素E2和E3不会使此类膜去极化。除了大肠菌素Ia诱导预先加载的铷、钠、磷酸盐或胆碱从脂质体中快速流出外,还会发生预先加载的蔗糖或6-磷酸葡萄糖的较慢流出。然而,经处理的脂质体不会泄漏菊粉或右旋糖酐,这表明E1和Ia的作用并非由于膜结构的普遍破坏。在完全没有膜电位的情况下观察到大肠菌素诱导的离子流出,这一事实表明这些大肠菌素对脂质体的作用不依赖于电压。这些结果提供了有力证据,表明大肠菌素Ia和E1使大肠杆菌细胞去极化是由于大肠菌素诱导的膜对离子的通透性增加。据推测,这是由大肠菌素分子与细菌细胞质膜的直接相互作用引起的。