Inward and outward rectifying potassium currents inSaccharomyces cerevisiae mediated by endogenous and heterelogously expressed ion channels
Disruption of genes encoding endogenous transport proteins inSaccharomyces cerevisiae has facilitated the recent cloning, by functional expression, of cDNAs encoding K+ channels and amino acid transporters from the plantArabidopsis thaliana [1–4]. In the present study, we demonstrate in whole-cell patch clamp experiments that the inability oftrk1Δtrk2Δ mutants ofS. 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 thetrk1Δtrk2Δ double-deletion mutant withKAT1 fromArabidopsis 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 atrk1 mutant withAKT1 fromA. thaliana.
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