Low-affinity potassium uptake by Saccharomyces cerevisiae is mediated by NSCI, a calcium-blocked non-specific cation channel

Previous descriptions by whole-cell patch clamping of the calcium-inhibited non-selective cation channel (NSC1) in the plasma membrane of Saccharomyces cerevisiae (H. Bihler, C.L. Slayman, A. Bertl, FEBS Lett. 432 (1998); S.K. Roberts, M. Fischer, G.K. Dixon, D.Sanders, J. Bacteriol. 181 (1999)) suggested that this inwardly rectifying pathway could relieve the growth inhibition normally imposed on yeast by disruption of its potassium transporters, Trk1p and Trk2p. Now, demonstration of multiple parallel effects produced by various agonists and antagonists on both NSC1 currents and growth (of trk1Deltatrk2Delta strains), has identified this non-selective cation pathway as the primary low-affinity uptake route for potassium ions in yeast. Factors which suppress NSC1-mediated inward currents and inhibit growth of trk1Deltatrk2Delta cells include (i) elevating extracellular calcium over the range of 10 muM-10 mM, (ii) lowering extracellular pH over the range 7.5-4, (iii) blockade of NSC1 by hygromycin B, and (iv) to a lesser extent by TEA(1). Growth of trk1Deltatrk2Delta cells is also inhibited by lithium and ammonium; however, these ions do not inhibit NSC1, but instead enter yeast cells via NSCL Growth inhibition by lithium ions is probably a toxic effect, whereas growth inhibition by ammonium ions probably results from competitive inhibition, i.e. displacement of intracellular potassium by entering ammonium. (C) 2002 Elsevier Science B.V. All rights reserved.