Light-induced membrane-potential increase, ATP synthesis, and proton uptake in Halobacterium halobium, R1mR catalyzed by halorhodopsin: Effects of N,N'-dicyclohexylcarbodiimide, triphenyltin chloride, and 3,5-di-tert-butyl-4-hydroxybenzylidenemalononitrile (SF6847).
Light-induced membrane-potential increase, ATP synthesis, and proton uptake in Halobacterium halobium, R1mR catalyzed by halorhodopsin: Effects of N,N'-dicyclohexylcarbodiimide, triphenyltin chloride, and 3,5-di-tert-butyl-4-hydroxybenzylidenemalononitrile (SF6847).
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光诱导的盐杆菌膜电位增加、ATP 合成和质子摄取，盐视紫红质催化的 R1mR：N,N-二环己基碳二亚胺、氯化三苯基锡和 3,5-二叔丁基-4-羟基苯亚甲基丙二腈的影响（
DOI：
10.1016/0003-9861(81)90067-9
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发表时间：
1981
影响因子：
3.9
通讯作者：
Y. Kaji
中科院分区：
文献类型：
--
作者：
Y. Mukohata;Y. Kaji
研究了N，N′-二环己基碳二亚胺（DCCD）、三苯基氯化锡（TPT）和3，5-二叔丁基-4-羟基亚苄基丙二腈（SP 6847）对含盐生盐杆菌R1 mR光依赖活性的影响。DCCD在光氧和暗氧条件下均能抑制ATP的合成，但不影响光诱导的质子吸收（ΔH+）。DCCD使暗厌氧条件下的膜电位降低，但在光照条件下，膜电位升高幅度与对照组相当（DCCD存在时，光依赖性膜电位增量Δψ明显增大）。TPT对ATP合成无明显影响，但对ΔH ~+和部分Δ H ~+有明显抑制作用。用DCCD处理R1 mR后，TPT几乎完全消除ΔH+，但仅部分消除Δ H+。SF6847使剩余的Δ λ崩塌，同时伴随质子掺入（pH升高）。这些结果导致了以下假设：（i）在R1 mR中，ATP是由H+-ATP酶合成的，H+-ATP酶与呼吸作用和/或盐视紫红质的光吸收作用耦合;（ii）大部分质子通过与H+-ATP酶不同的机制掺入光中，但由盐视紫红质产生的Δ H驱动;（iii）TPT在该系统中起氯/氢交换剂的作用;（iv）解偶联剂SF 6847响应于Δ λ将质子携带到细胞中。
The effects ofN,N′-dicyclohexylcarbodiimide (DCCD), triphenyltin chloride (TPT), and 3,5-di-tert-butyl-4-hydroxybenzylidenemalonomtrile (SP6847) were tested on the light-dependent activities ofHalobacterium halobiumR1mR which contains a new retinal protein pigment designated as halorhodopsin but no bacteriorhodospin. DCCD inhibited ATP synthesis either in the light- or in the dark-aerobic conditions without affecting the light-induced proton uptake (ΔH+). Although DCCD lowered the membrane potential under dark-anaerobic conditions, the potential increased in the light as high as the control (the light-dependent membrane potential increment Δψ became apparently larger in the presence of DCCD). TPT had negligible effect on ATP synthesis both in the dark or in the light but inhibited markedly ΔH+and partly Δψ. After R1mR was treated with DCCD, TPT abolished ΔH+almost completely but Δψ only partly. The remaining Δψ was collapsed by SF6847 with a concomitant proton incorporation (pH increase). These results led to the following postulations: (i) In R1mR, ATP is synthesized by a H+-ATPase coupled either to respiration and/or light energization by halorhodopsin; (ii) the majority of protons are incorporated in the light by a mechanism which differs from H+-ATPase but is driven by the Δψ generated by halorhodopsin; (iii) TPT acts in this system as a chloride/hydroxide exchanger; (iv) the uncoupler SF6847 carries protons into cells in response to Δψ.