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      Origin, cellular expression, and cybrid transmission of mitochondrial CAP-R, PYR-IND, and OLI-R mutant phenotypes.

      Somatic cell genetics
      Animals, Cell Line, Chloramphenicol, pharmacology, Cricetinae, Cricetulus, DNA, Mitochondrial, genetics, Drug Resistance, Genes, Hybrid Cells, metabolism, Mice, Mitochondria, Mutation, Oligomycins, Phenotype, Pyruvates, Pyruvic Acid

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          Abstract

          Chloramphenicol-resistant (CAP-R) mouse and Chinese hamster lines were isolated in a single selection step in drug medium containing pyruvate. Cellular expression of the CAP-R phenotype required pyruvate--or an appropriate substitute--as a nutritional supplement. Subclone lines which were pyruvate independent (PYR-IND) arose in second-step selections at a high frequency. CAP-R PYR-IND Chinese hamster mutants could be directly isolated in single-step selections but at a very low frequency. Subclone lines (OLI-R) which were cross-resistant to oligomycin were isolated in a third selection cycle. The PYR-IND and OLI-R phenotypes were cotransmitted with the CAP-R mtDNA mutation but were expressed at the cellular level only if the number of mutant mitochondrial genomes exceeded a minimum threshold value. Analysis of a mtDNA restriction fragment alteration in one series of mutants supported this model. Threshold limits for cellular expression of mitochondrial mutant phenotypes are likely to be a general phenomenon and will constrain models of the origin and segregation of mtDNA mutations.

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