Open AccessSaccharomyces cerevisiae mutants sensitive to the antimalarial and antiarrhythmic drug, quinidine
Author(s) -
Conklin Douglas S.,
Culbertson Michael R.,
Kung Ching
Publication year - 1994
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.1994.tb06892.x
Subject(s) - quinidine , complementation , saccharomyces cerevisiae , mutant , biology , allele , phenotype , quinine , genetics , mutation , pharmacology , gene , malaria , immunology
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 α but not a cells, due to a defect in α‐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.