Relationship of the Escherichia coli TrkA system of potassium ion uptake with the F sub(0)F sub(1)-ATPase under growth conditions without anaerobic or aerobic respiration

K super(+) uptake by the Escherichia coli TrkA system is unusual in that it requires both ATP and Delta mu sub(H) super(+); a relation with H super(+) circulation through the membrane is therefore suggested. The relationship of this system with the F sub(0)F sub(1)-ATPase was studied in intact cells grown under different conditions. A significant increase of the N,N'-dicyclohexylcarbodiimide(DCCD)-inhibited H super(+) efflux through the F sub(0)F sub(1) by 5 mM K super(+), but not by N super(+) added into the potassium-free medium was revealed only in fermenting wild-type or parent cells, that were grown under anaerobic conditions without anaerobic or aerobic respiration and with the production of H sub(2). Such an increase disappeared in the Delta unc or the trkA mutants that have altered F sub(0)F sub(1) or defective TrkA, respectively. This finding indicates a closed relationship between TrkA and F sub(0)F sub(1), with these transport systems being associated in a single mechanism that functions as an ATP-driven H super(+)-K super(+)-exchanging pump. A DCCD-inhibited H super(+)-K super(+)-exchange through these systems with the fixed stoichiometry of H super(+) and K super(+) fluxes (2H super(+)/K super(+)) and a higher K super(+) gradient between the cytoplasm and the external medium were also found in these bacteria. They were not observed in cells cultured under anaerobic conditions in the presence of nitrate or under aerobic conditions with respiration and without production of H sub(2). The role of anaerobic or aerobic respiration as a determinant of the relationship of the TrkA with the F sub(0)F sub(1) is postulated. Moreover, an increase of DCCD-inhibited H super(+) efflux by added K super(+), as well as the characteristics of DCCD-sensitive H super(+)-K super(+)-exchange found in a parent strain, were lost in the arcA mutant with a defective Arc system, suggesting a repression of enzymes in respiratory pathways. In addition, K super(+) influx in the latest mutant was not markedly changed by valinomycin or with temperature. The arcA gene product or the Arc system is proposed to be implicated in the regulation of the relationship between TrkA and F sub(0)F sub(1).