Potassium transport in<i>Escherichia coli</i>: sodium is not a substrate of the potassium uptake system TrkA

Abstract

In Escherichia coli cells depleted of both sodium and potassium, the potassium uptake system TrkA mediated a slow, electrogenic uptake of potassium. Electroneutrality was maintained by the extrusion of protons. Internal, but not external sodium stimulated potassium uptake. This extra uptake was coupled to a stoichiometric extrusion of sodium. Triethanolamine also stimulated potassium uptake, presumably by increasing the cytoplasmic buffer capacity. These results are taken to mean that sodium is not a substrate of the TrkA system, but stimulates TrkA activity by facilitating the reentry of protons through the sodium-proton antiporter, and thereby preventing a prohibitive increase in cytoplasmic pH.