title: ATP generation during reduced inorganic sulfur compound oxidation by Acidithiobacillus caldus is exclusively due to electron transport phosphorylation.
abstract: The synthesis of adenosine 5-triphosphate (ATP) (increase in phosphorylation potential) during the oxidation of reduced inorganic sulfur compounds was studied in the moderately thermophilic acidophileAcidithiobacillus caldus (strain KU) (formerly Thiohacillus caldus). The phosphorylation potential increased during the oxidation of all reduced inorganic sulfur compounds tested compared with resting cells. The generation of ATP in whole cells was inhibited by the F0F1 ATPase inhibitor oligomycin, electron transport chain inhibitors, valinomycin and potassium ions. There was no increase in the phosphorylation potential, nor synthesis of ATP. in the absence of electron transport. An apparent lack of substrate-level phosphorylation was indicated by the lack of adenosine 5-phosphosulfate reductase in tetrathionate-grown At. caldus. Studies were also performed on the synthesis of ATP by membrane vesicles of At. caldus when presented with an artificial proton gradient. Complete inhibition of ATP synthesis in these vesicles occurred when they were loaded with N,N-dicyclohexylcarbodiimide (DCCD), but not when they were loaded with oligomycin, vanadate or electron transport chain inhibitors. The data presented here suggest that during the oxidation of reduced inorganic sulfur compounds by At. caldus, all ATP is synthesized by oxidative phosphorylation via a membrane-bound F0F1 ATPase driven by a proton gradient.
authors.affiliation: Department of Microbiology, Umeå University, Sweden.
authors.forename: Mark
authors.initials: M
authors.lastname: Dopson
authors.forename: E Börje
authors.initials: EB
authors.lastname: Lindström
authors.forename: Kevin B
authors.initials: KB
authors.lastname: Hallberg
mesh_terms: D000255:Adenosine Triphosphate / Q000096:biosynthesis*; D004579:Electron Transport / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D009840:Oligomycins / Q000494:pharmacology; D010084:Oxidation-Reduction; D010088:Oxidoreductases / Q000378:metabolism; D050862:Oxidoreductases Acting on Sulfur Group Donors; D010766:Phosphorylation; D011188:Potassium / Q000494:pharmacology; D006180:Proton-Translocating ATPases / Q000037:antagonists & inhibitors / Q000378:metabolism; D013455:Sulfur / Q000378:metabolism*; D013855:Thiobacillus / Q000187:drug effects / Q000378:metabolism*; D014634:Valinomycin / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D009840:Oligomycins; D014634:Valinomycin; D013455:Sulfur; D000255:Adenosine Triphosphate; D010088:Oxidoreductases; D050862:Oxidoreductases Acting on Sulfur Group Donors; C019618:adenylylsulfate reductase; D006180:Proton-Translocating ATPases; D011188:Potassium