Segregational respiratory-deficient mutants of a "petite negative" yeast Schizosaccharomyces pombe 972h-

Journal of Bacteriology
|October 1, 1970
PubMed

Insights

Researchers explored respiratory-deficient mutants in yeast. Acriflavine and ethidium bromide induced unstable petites, while segregational mutants showed altered mitochondrial structures and inhibited respiration.

Area of Science:

  • Molecular and Cellular Biology
  • Yeast Genetics
  • Mitochondrial Research

Background:

  • Investigating respiratory-deficient mutants in the fission yeast Schizosaccharomyces pombe is crucial for understanding mitochondrial function.
  • Previous studies utilized chemical mutagens to induce mutations affecting cellular respiration.

Purpose of the Study:

  • To characterize respiratory-deficient mutants of Schizosaccharomyces pombe induced by acriflavine and ethidium bromide.
  • To isolate and analyze segregational respiratory-deficient mutants with resistance to specific inhibitors.

Main Methods:

  • Treatment of Schizosaccharomyces pombe with acriflavine and ethidium bromide to induce mutations.
  • Isolation of respiratory-deficient mutants resistant to cobalt sulfate, 2,4-dinitrophenol, decamethylene diguanidine, and benzimidazole.
  • Analysis of mitochondrial morphology and respiratory function in isolated mutant strains.

Main Results:

  • Acriflavine and ethidium bromide treatments did not yield viable respiratory-deficient mutants but induced unstable petites.
  • Segregational mutants resistant to cobalt sulfate exhibited deficiencies in cytochrome a + a(3), reduced respiration, and altered mitochondrial membrane structures.
  • Mutants resistant to other inhibitors showed no significant changes in mitochondrial structure or function, except for a benzimidazole-resistant mutant unable to grow on glycerol.

Conclusions:

  • The chemical mutagens acriflavine and ethidium bromide primarily induce unstable petite mutations in Schizosaccharomyces pombe.
  • Segregational respiratory deficiency in yeast can lead to distinct alterations in mitochondrial morphology and respiratory chain components.
  • Specific inhibitor resistance in yeast mutants can reveal complex interactions between mitochondrial function, respiration, and metabolic pathways.

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