The regulation of potassium fluxes for the adjustment and maintenance of potassium levels in Escherichia coli.
The regulation of K+ fluxes has been studied in Escherichia coli after depletion of K+ by an osmotic shock or at steady state of potassium accumulation. In the absence of a carbon source, bacteria accumulate K+ to an intracellular level near 0.1 M about half of actively metabolizing cells. During uptake the rate of net unidirectional influx decreased with time down to zero as a plateau was reached and no efflux was observed. Accumulated K+ was not exchanged with external K+ under these conditions. In the presence of a carbon source bacteria took up potassium to an intracellular concentration near 0.2 M. Efflux was delayed: it started only when 50% of final cellular K+ has been taken up. At steady state cellular K+ was exchangeable with external K+. The removal of the carbon source or the addition of respiratory inhibitors immediately stopped the K+ influx but did not affect efflux until the cellular K+ concentration has dropped to a level near 0.1 M; residual potassium was no longer exchangeable with external potassium. Maintaining such an impermeability to K+ ion does not require energy (delta psi or ATP), even though residual K+ is concentrated 100-fold compared to K+ in the medium. These results suggest that K+ efflux is dependent on active metabolism and on the concentration of intracellular K+ above a threshold. Unidirectional influx is also regulated by intracellular K+ according to a different concentration dependence. It appears that the trkA system, which is the only functional system under these experimental conditions is not a 'pump and leak' type of transport system.
D001692:Biological Transport; D002244:Carbon / Q000494:pharmacology; D004734:Energy Metabolism / Q000187:drug effects; D004926:Escherichia coli / Q000378:metabolism*; D009997:Osmotic Pressure; D011188:Potassium / Q000378:metabolism*
D002244:Carbon; D011188:Potassium