Abstract
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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This work was supported by a grant from theForschungsgemeinschaft (A.B.), TheU.S. Department of Energy (c.L.S.), The U.S. National Science Foundation (R.F.G.) Lisboa, Portugal.
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Bertl, A., Anderson, J.A., Slayman, C.L. et al. Inward and outward rectifying potassium currents inSaccharomyces cerevisiae mediated by endogenous and heterelogously expressed ion channels. Folia Microbiol 39, 507–509 (1994). https://doi.org/10.1007/BF02814074
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DOI: https://doi.org/10.1007/BF02814074