"Killer" character does not influence the transmission of mitochondrial genes in Saccharomyces cerevisiae.
Three cytoplasmic genetic elements have been shown to be separate from mitochondrial deoxyribonucleic acid (DNA), [rho], in Saccharomyces cerevisiae: the killer character [k], omicron-DNA, and psi [psi]. Griffiths has suggested genetic interactions between [VENR] and [TETR] mutants possibly located on omicron-DNA and mitochondrial genetic markers, but possible interactions between the best characterized of the three, the killer character, and mitochondrial DNA have not been investigated. To test this we isolated cycloheximide-induced nonkiller segregants (NKS) of killer cells with suitable genetic markers and mated them in [k] x [k], [k] x [k], and (NKS) x (NKS) combinations. No differences in quantitative mitochondrial marker transmission between these groups were found in crosses illustrating the mitochondrial phenomena of bias, polarity, and suppressiveness. Our studies show that no intercellular interactions between [k] and (NKS) cells influence mitochondrial transmission genetics. Intracellular interactions between the smaller double-stranded ribonucleic acid of [k] and mitochondrial DNA also were not detected.
D002701:Chloramphenicol / Q000494:pharmacology; D003227:Conjugation, Genetic; D003433:Crosses, Genetic; D003513:Cycloheximide / Q000494:pharmacology; D004247:DNA; D004352:Drug Resistance, Microbial; D004917:Erythromycin / Q000494:pharmacology; D005111:Extrachromosomal Inheritance; D005796:Genes; D008928:Mitochondria; D009154:Mutation; D010303:Paromomycin / Q000494:pharmacology; D010641:Phenotype; D012441:Saccharomyces cerevisiae / Q000187:drug effects; D013489:Suppression, Genetic
D010303:Paromomycin; D004917:Erythromycin; D002701:Chloramphenicol; D004247:DNA; D003513:Cycloheximide