Answers are grounded in this paper and cite their sources.
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.
No takes yet. Share an insight, caveat, or question.
Meury et al. (1981) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: