Saccharomyces cerevisiae mutants sensitive to the antimalarial and antiarrhythmic drug, quinidine.
Mutations at three loci in Saccharomyces cerevisiae have been shown to confer increased sensitivity to the antimalarial and antiarrhythmic alkaloid, quinidine. Two of these groups are composed of strains carrying recessive mutations, the other group contains two dominant alleles. The largest complementation group has been designated QDS1, for increased quinidine-sensitivity. Exposure of qds1 cells to lethal concentrations of quinidine results in a novel small-budded terminal morphology in about 70% of the cells in the culture. Strains which carry qds1 alleles share other pleiotropic phenotypes. qds1 mutants are incapable of mating as alpha but not a cells, due to a defect in alpha-factor production. Homozygous diploid qds1 strains cannot sporulate. Genetic evidence indicates that QDS1 is allelic to KEX2, a precursor processing protease. Loss of QDS1/KEX2 function results in quinidine sensitivity.
Laboratory of Molecular Biology, University of Wisconsin-Madison 53706.
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D000483:Alleles; D004351:Drug Resistance; D009154:Mutation; D043484:Proprotein Convertases; D011802:Quinidine / Q000494:pharmacology*; D012441:Saccharomyces cerevisiae / Q000187:drug effects* / Q000235:genetics; D029701:Saccharomyces cerevisiae Proteins; D013381:Subtilisins / Q000502:physiology
D029701:Saccharomyces cerevisiae Proteins; D043484:Proprotein Convertases; D013381:Subtilisins; C058751:KEX2 protein, S cerevisiae; D011802:Quinidine