The plasma membrane electrical potential plays an essential role in all cells, modulating the transport of charged molecules through pumps, channels, uniports and cotransport systems [1]. In Saccharomyces cerevisiae, the plasma membrane potential is primarily determined by the two major electrogenic transporters: the H+-ATPase encoded by the essential PMA1 gene [2] and the Trk high affinity potassium uptake system encoded by the TRK1 and TRK2 genes [3–5]. The proton-pumping activity of Pma1 generates an electrochemical proton gradient and the Trk system is a major consumer of the membrane potential because of the high rates of K+ uptake. Alterations in the expression and/or activities of Pma1 or Trk1–Trk2 would affect the membrane potential and, consequently, the uptake of nutrients and toxic cations [6,7]. Therefore, the regulation of