Brewer G J
Biochemistry. 1976 Apr 6;15(7):1387-92. doi: 10.1021/bi00652a006.
The bacterial protein colicin K, when added to sensitive Escherichia coli in the presence of 3,3'-dihexyloxacarbocyanine, cuases a doubling in fluorescence of the probe. Glucose and oxygen cause a decreased fluorescence while anoxia and cyanide cause a rise in fluorescence. These results in conjunction with the work of other laboratories suggest that colicin K causes a depolarization of the transmembrane electrical potential. Fluorescence in the absence of colicin K was relatively independent of KCl, NaCl, and MgCl2 concentrations below 0.1 M. Although colicin K caused rapid efflux of the K+ analogue 86Rb+, the fluorescence rise was only partially blocked by 0.13 M KCl. The level of fluorescence caused by the action of colcin K was inversely proportional to the logarithm of the concentration of MgCl2 over the range of 2 muM to 4 mM. This suggests that a Nernst electrochemical potential for an anion can counteract a membrane depolarization caused by colcin. After colcin K action, the fluorescence of the carbocyanine could be further increased by anoxia or cyanide. The distribution of the weak base dimethyloxazolidinedione indicated that the pH in the interior of aerobic E. coli supplied with lactate was alkaline by 0.1 unit and unaffected by colicin. These results suggest that colicin K does not completely depolarize the membrane potential and does not interfere with the component of membrane energization generated by electron transport. Colicin K does not act as a cationophore. The partial depolarization of the membrane may account for the inhibition of active solute transport caused by colicin K.
细菌蛋白大肠菌素K在3,3'-二己基氧杂羰花青存在的情况下添加到敏感的大肠杆菌中时,会使探针的荧光增强一倍。葡萄糖和氧气会导致荧光减弱,而缺氧和氰化物会导致荧光增强。这些结果与其他实验室的工作相结合,表明大肠菌素K会导致跨膜电势去极化。在没有大肠菌素K的情况下,荧光相对独立于浓度低于0.1 M的KCl、NaCl和MgCl2。尽管大肠菌素K导致K+类似物86Rb+快速外流,但0.13 M KCl仅部分阻断了荧光增强。在2 μM至4 mM的范围内,由大肠菌素K作用引起的荧光水平与MgCl2浓度的对数成反比。这表明阴离子的能斯特电化学势可以抵消大肠菌素引起的膜去极化。在大肠菌素K作用后,花青的荧光可通过缺氧或氰化物进一步增强。弱碱二甲基恶唑烷二酮的分布表明,供应乳酸的需氧大肠杆菌内部的pH值呈碱性,比外部高0.1个单位,且不受大肠菌素影响。这些结果表明,大肠菌素K不会使膜电位完全去极化,也不会干扰由电子传递产生的膜能量化成分。大肠菌素K不是阳离子载体。膜的部分去极化可能解释了大肠菌素K对活性溶质转运的抑制作用。