Abstract
Saccharomyces cerevisiae cells containing a deletion of TRK1, the gene encoding the high affinity potassium transporter, retain only low affinity uptake of this ion and consequently lose the ability to grow in media containing low levels (0.2 mM) of potassium. Using a trk1 delta strain, we selected spontaneous Trk+ pseudorevertants that regained the ability to grow on low concentrations of potassium. The revertants define three unlinked extragenic suppressors of trk1 delta. Dominant RPD2 mutations and recessive rpd1 and rpd3 mutations confer increased potassium uptake in trk1 delta cells. Genetic evidence suggests that RPD2 mutations are alleles of TRK2, the putative low affinity transporter gene, whereas rpd1 and rpd3 mutations increase TRK2 activity: (1) RPD2 mutations are closely linked to trk2, and (2) trk2 mutations are epistatic to both rpd1 and rpd3. rpd1 maps near pho80 on chromosome XV and rpd3 maps on the left arm of chromosome XIV, closely linked to kre1.
MeSH Terms
Alleles
Biological Transport
Carrier Proteins/genetics
Chromosome Mapping
Chromosomes, Fungal
Epistasis, Genetic
Genes, Dominant
Genes, Fungal
Genetic Complementation Test
Hydrogen-Ion Concentration
Mutation
Phenotype
Potassium/metabolism
Rubidium/metabolism
Saccharomyces cerevisiae/genetics,growth & development,metabolism
Chemicals
Carrier Proteins
Rubidium
Potassium
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Vidal M
Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern University, Evanston, Illinois 60208.
Buckley A M
Hilger F
Gaber R F
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