Gradmann D, Slayman C L
J Membr Biol. 1975 Aug 29;23(2):181-212. doi: 10.1007/BF01870250.
The presence of the poky mutation in Neurospora crassa produces mitochondria which are defective in cytochromes b and aa3 but which compensate by means of an alternate, cyanide-insensitive oxidase. As previously reported (Slayman, Rees, Orchard & Slayman, J. Biol. Chem., 250:396, 1975) cyanide blockade of the poky strain carrying the partial suppressor f results in a metabolic downshift of only 56%, compared with a downshift of 98% in wild-type Neurospora; the downshift is accompanied by exponential decay of ATP in the wild type, but by an undershoot and monotonic recovery of ATP in poky f. Whereas the membrane potential declines with ATP in wild-type Neurospora, it oscillates near the resting level (ca. -- 185 mV) in poky f. Oscillations begin with a depolarizing swing of 30--100 mV, followed by slight hyperpolarization, then by 2--4 damped cycles having a frequency near 1/min. Similar oscillations arise with antimycin, salicyl hydroxamic acid, and several uncoupling agents, and depend on partial maintenance of respiration through either the defective cytochrome chain or the alternate oxidase. Small oscillations (maximally +/- 30% of the control value) in membrane conductance also occur, roughly in phase with the oscillations of membrane potential. The amplitude of these, in comparison with the nonlinearity of the normal current-voltage relationship for the membrane, strongly suggests that they arise as a secondary consequence of the voltage changes. Therefore, since it has previously been argued (Slayman, Long & Lu, J. Membrane Biol. 14:305, 1973) that most of the resting membrane potential in the organism arises from active extrusion of H+ ions, the simolest interpretation of the cyanide-induced voltage oscillations is that current through the H+ pump is modulated cyclically. The ultimate mechanism for this modulation is unresolved, but could plausible involve a metabolic feedback system, oscillations of intracellular pH, or both. In many respects the observed voltage oscillations resemble the well-known oscillations of mitochondrial H+ flux which are produced by sudden metabolic shifts.
粗糙脉孢菌中迟缓突变的存在会产生线粒体，这些线粒体在细胞色素b和aa3方面存在缺陷，但可通过一种替代的、对氰化物不敏感的氧化酶进行补偿。如先前报道（斯莱曼、里斯、奥查德和斯莱曼，《生物化学杂志》，250:396，1975），携带部分抑制因子f的迟缓菌株经氰化物阻断后，代谢下降仅56%，而野生型粗糙脉孢菌的代谢下降为98%；野生型中代谢下降伴随着ATP呈指数衰减，而迟缓f型中ATP则出现下冲并单调恢复。在野生型粗糙脉孢菌中，膜电位随ATP下降，而在迟缓f型中，膜电位在静息水平（约-185 mV）附近振荡。振荡始于30 - 100 mV的去极化摆动，随后是轻微的超极化，然后是2 - 4个阻尼周期，频率接近1/分钟。抗霉素、水杨羟肟酸和几种解偶联剂也会引发类似振荡，且依赖于通过有缺陷的细胞色素链或替代氧化酶对呼吸作用的部分维持。膜电导也会出现小振荡（最大为对照值的+/- 30%），大致与膜电位振荡同步。与膜正常电流 - 电压关系的非线性相比，这些振荡的幅度强烈表明它们是电压变化的次要结果。因此，由于先前有人认为（斯莱曼、朗和卢，《膜生物学杂志》14:305，1973）生物体中的大部分静息膜电位源于H⁺离子的主动外排，对氰化物诱导的电压振荡最简单的解释是通过H⁺泵的电流受到周期性调制。这种调制的最终机制尚未解决，但可能合理地涉及代谢反馈系统、细胞内pH值振荡或两者兼有。在许多方面，观察到的电压振荡类似于由突然的代谢转变产生的著名的线粒体H⁺通量振荡。
