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The acidophilic bacterium PW2 possessed a delta pH of ca. 1.9 and a delta psi of 0 mV, corresponding to a proton motive force (delta p) of--114 mV. Protonophore-treated cells possessed little delta p but a delta pH of ca. 1.5, as measured by salicylic acid distribution or pH measurement of cell lysates. Starving PW2 cells continued to possess a delta pH of ca. 1.7, but exhibited converse changes in delta psi and delta p, with the former rising to +80 to +100 mV and the latter dropping essentially to 0; progressive loss of respiration, cellular ATP, and culture viability accompanied these changes. Thus, the protonophore-treated or starving PW2 cells attained an H+ electrochemical equilibrium. Net H+ influx resulting from declining respiration probably accounted for the increased delta psi in these cells; indeed, when respiration was progressively inhibited in active cells, there was increasing transient H+ influx and a proportional increase in delta psi. This transient H+ influx was sufficient to lethally acidify the cytoplasm, but for a buffering capacity of 85 nmol of H+/mg of protein per pH unit. Thus, the linkage of the transient H+ influx with the rise in the delta psi and the cytoplasmic buffering capacity play central roles in acidophilism, and it is conceivable that the same impermeant cellular macromolecule(s) accounts for both. If so, the delta psi would be a Donnan potential that in active cells is offset by energy-dependent H+ extrusion.

Mechanism of delta pH maintenance in active and inactive cells of an obligately acidophilic bacterium