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. trkI Δ trk2 mutants require up to tenfold higher concentrations of K+ to exhibit normal growth compared to trk1Δ TRK2 cells. K+ and 86Rb+ transport assays demonstrate that the mutant phenotype is due to effective 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 (trk1Δ 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.
Original language | English (US) |
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Pages (from-to) | 305-312 |
Number of pages | 8 |
Journal | Genetics |
Volume | 125 |
Issue number | 2 |
State | Published - Jun 14 1990 |
ASJC Scopus subject areas
- Genetics