Inward and outward rectifying potassium currents in Saccharomyces cerevisiae mediated by endogenous and heterelogously expressed ion channels

Disruption of genes encoding endogenous transport proteins in Saccharomyces cerevisiae has facilitated the recent cloning, by functional expression, of cDNAs encoding K⁺ channels and amino acid transporters from the plant Arabidopsis thaliana [1–4]. In the present study, we demonstrate in whole-cell patch clamp experiments that the inability of trk1Δtrk2Δ mutants of S. cerevisiae to grow on submillimolar K⁺ correlates with the lack of K⁺ inward currents, which are present in wild-type cells, and that transformation of the trk1Δtrk2Δ double-deletion mutant with KAT1 from Arabidopsis thaliana restores this phenotype by encoding a plasma membrane protein that allows large K⁺ inward currents. Similar K⁺ inward currents are induced by transformation of a trk1 mutant with AKT1 from A. thaliana.