K+ uptake by the Escherichia coli TrkA system is unusual in that it requires both ATP and ΔμH; a relation withH+ circulation through the membrane is thereforesuggested. The relationship of this system with the F0F1-ATPase was studied in intact cells grownunder different conditions. A significant increase of the N,N'-dicyclohexylcarbodiimide(DCCD)-inhibitedH+ efflux through the F0F1 by 5 mMK+, but not by Na+ added into thepotassium-free medium was revealed only in fermenting wild-type orparent cells, that were grown under anaerobic conditions withoutanaerobic or aerobic respiration and with the production of H2. Such an increase disappeared in the Δunc or the trkA mutants that have alteredF0F1 or defective TrkA, respectively. This finding indicates a closed relationship between TrkA andF0F1, with these transport systems beingassociated in a single mechanism that functions as an ATP-driven H+–K+-exchanging pump. ADCCD-inhibited H+–K+-exchangethrough these systems with the fixed stoichiometry of H+and K+ fluxes(2H+/K+) and a higherK+ gradient between the cytoplasm and the externalmedium were also found in these bacteria. They were not observed incells cultured under anaerobic conditions in the presence of nitrate orunder aerobic conditions with respiration and without production of H2. The role of anaerobic or aerobic respiration as adeterminant of the relationship of the TrkA with the F0F1 is postulated. Moreover, an increase of DCCD-inhibited H+ efflux by added K+, aswell as the characteristics of DCCD-sensitiveH+–K+-exchange found in a parentstrain, were lost in the arcA mutant with a defective Arc system, suggesting a repression of enzymes in respiratorypathways. In addition, K+ influx in the latest mutantwas not markedly changed by valinomycin or with temperature. The arcA gene product or the Arc system is proposed to beimplicated in the regulation of the relationship between TrkA and F0F1.

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