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.
Membrane Voltage Wildtype Cell Maltose Medium Gene TRK1 Native Gene Product
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