Open AccessPotassium transport in Escherichia coli : sodium is not a substrate of the potassium uptake system TrkA
Author(s) -
Bakker Evert P.,
Kroll Rohan G.,
Booth Ian R.
Publication year - 1984
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.1984.tb01081.x
Subject(s) - potassium , sodium , chemistry , antiporter , substrate (aquarium) , triethanolamine , escherichia coli , biophysics , biochemistry , chromatography , biology , analytical chemistry (journal) , organic chemistry , ecology , gene
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.