Molecular and General Genetics MGG

, Volume 149, Issue 1, pp 33-42

First online:

Assembly of the mitochondrial membrane system XVIII

Genetic loci on mitochondrial DNA involved in cytochrome b biosynthesis
  • Alexander TzagoloffAffiliated withThe Public Health Research Institute of the City of New York, Inc.
  • , Francoise FouryAffiliated withThe Public Health Research Institute of the City of New York, Inc.
  • , Anna AkaiAffiliated withThe Public Health Research Institute of the City of New York, Inc.

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  1. 1.

    Fourteen cytoplasmic mutants of Saccharomyces cerevisiae with a specific deficiency of cytochrome b have been studied. The mutations have been shown to occur in two separate genetic loci, COB 1 and COB 2. These loci can be distinguished by mitxmit crosses. Pairwise crosses of cytochrome b mutants belonging to different loci yield 4–6% wild type recombinants corresponding to recombinational frequencies of 8–12%. In intra-locus crosses, the recombinational frequencies range from 1% to less than 0.01%. The two loci can also be distinguished by mit × ρ crosses. Twenty ρ testers have been isolated of which ten preferentially restore mutations in COB 1 and ten others in COB 2.

  2. 2.

    The COB 1 and COB 2 loci have been localized on mitochondrial DNA between the two antibiotic resistance loci OLI 1 and OLI 2 in the order OLI 2-COB 2-COB 1-OLI 1. The results of mitxmit and mit × ρ crosses have also been used to map the cytochrome b mutations relative to each other. The maps obtained by the two independent methods are in good agreement.

  3. 3.

    Mutations in COB 1 have been found to be linked to the OLI1 locus in some but not in other strains of S. cerevisiae. This evidence suggests that there may be a spacer region between the two loci whose length varies from strain to strain.

  4. 4.

    Two mutations in COB 2 have been found to cause a loss of a mitochondrial translation product corresponding to the cytochrome b apoprotein. Instead of the wild type protein the mutants have a new low-molecular weight product which is probably a fragment of cytochrome b. The fact that the mutations revert suggests that they are nonsense mutations in the structural gene of cytochrome b.