Abstract
TRK1, the gene encoding the high affinity K(+) transporter in Saccharomyces cerevisiae, is nonessential due to the existence of a functionally independent low affinity transporter. To identify the gene(s) encoding the low affinity K(+) transporter, we screened trk1 Δ cells for mutants (Kla(-)) that require higher concentrations of K(+) in the medium to support growth. trk1 Δ trk2 mutants require up to tenfold higher concentrations of K(+) to exhibit normal growth compared to trk1 Δ TRK2 cells. K(+) and (86)Rb(+) transport assays demonstrate that the mutant phenotype is due to defective K(+) transport (uptake). Each of 38 independent mutants contains a mutation in the same gene, TRK2. Cells deficient for both high and low affinity K(+) transport (trk1 Δ trk2) exhibit hypersensitivity to low extracellular pH that can be suppressed by high concentrations of K(+) but not Na(+). TRK1 completely suppresses both the K(+) transport defect and low pH hypersensitivity of trk2 cells, suggesting that TRK1 and TRK2 are functionally independent.
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