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.
|Original language||English (US)|
|Number of pages||3|
|Journal||Folia Microbiologica: Official Journal of the Institute of Microbiology, Academy of Sciences of the Czech Republic|
|State||Published - Nov 1994|
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