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首页> 美国卫生研究院文献>Journal of Bacteriology >Stimulation of Menaquinone-Dependent Electron Transfer in the Respiratory Chain of Bacillus subtilis by Membrane Energization
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Stimulation of Menaquinone-Dependent Electron Transfer in the Respiratory Chain of Bacillus subtilis by Membrane Energization

机译：通过膜能量刺激枯草芽孢杆菌呼吸链中依赖于对甲醌的电子转移

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摘要

At a pH of ≤7, respiration of Bacillus subtilis cells on endogenous substrates shut down almost completely upon addition of an uncoupler (carbonyl cyanide m-chlorophenylhydrazone [CCCP]) and a K+-ionophore (valinomycin). The same effect was observed with cell spheroplasts lacking the cell wall. The concentration of CCCP required for 50% inhibition of the endogenous respiration in the presence of K+-valinomycin was below 100 nM. Either CCCP or valinomycin alone was much less efficient than the combination of the two. The inhibitory effect was easily reversible and depended specifically on the H+ and K+ concentrations in the medium. Similar inhibition was observed with respect to the reduction of the artificial electron acceptors 2,6-dichlorophenolindophenol (DCPIP) and N,N,N′,N′-tetramethyl-p-phenylenediamine cation (TMPD+), which intercept reducing equivalents at the level of menaquinol. Oxidation of the reduced DCPIP or TMPD in the bacterial cells was not sensitive to uncoupling. The same loss of the electron transfer activities as induced by the uncoupling was observed upon disruption of the cells during isolation of the membranes; the residual activities were not further inhibited by the uncoupler and ionophores. We conclude that the menaquinone-dependent electron transfer in the B. subtilis respiratory chain is facilitated, thermodynamically or kinetically, by membrane energization. A requirement for an energized state of the membrane is not a specific feature of succinate oxidation, as proposed in the literature, since it was also observed in a mutant of B. subtilis lacking succinate:quinone reductase as well as for substrates other than succinate. Possible mechanisms of the energy-dependent regulation of menaquinone-dependent respiration in B. subtilis are discussed.
机译：在pH≤7的条件下，添加解偶联剂（羰基氰化物间氯苯基hydr [CCCP]）和K + 离子载体（缬霉素）后，内源性底物上枯草芽孢杆菌细胞的呼吸几乎完全关闭。 。对于缺少细胞壁的细胞原生质球，观察到相同的效果。在K + -valinomycin存在下，抑制内源性呼吸50％所需的CCCP浓度低于100 nM。单独使用CCCP或缬氨霉素的效率均低于两者的组合。抑制作用易于逆转，具体取决于培养基中H + 和K + 的浓度。在减少人工电子受体2,6-二氯苯酚吲哚酚（DCPIP）和N，N，N'，N'-四甲基-对苯二胺阳离子（TMPD + ）方面也观察到类似的抑制，可拦截甲萘醌水平的还原当量。细菌细胞中还原的DCPIP或TMPD的氧化对解偶联不敏感。在分离膜期间破坏细胞时，观察到了与解偶联所引起的相同的电子传递活性损失。残留的活性不再受到解偶联剂和离子载体的抑制。我们得出的结论是，通过膜激发，热力学或动力学促进了枯草芽孢杆菌呼吸链中依赖甲萘醌的电子转移。如在文献中所提出的，对膜的激发态的需求不是琥珀酸氧化的特定特征，因为在缺乏琥珀酸：醌还原酶的枯草芽孢杆菌的突变体以及除了琥珀酸以外的底物上也观察到了这一点。讨论了枯草芽孢杆菌中依赖于甲萘醌的呼吸的能量依赖性调节的可能机制。

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