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Prion-dependent switching between respiratory competence and deficiency in the yeast nam9-1 mutant.

Nam9p is a protein of the mitochondrial ribosome. The respiration-deficient Saccharomyces cerevisiae strain MB43-nam9-1 expresses Nam9-1p containing the point mutation S82L. Respiratory deficiency correlates with a decrease in the steady level of some mitochondrially encoded proteins and the complete lack of mitochondrially encoded cytochrome oxidase subunit 2 (Cox2). De novo synthesis of Cox2 in MB43-nam9-1 is unaffected, indicating that newly synthesized Cox2 is rapidly degraded. Respiratory deficiency of MB43-nam9-1 is overcome by transient overexpression of HSP104, by deletion of HSP104, by transient exposure to guanidine hydrochloride, and by expression of the C-terminal portion of Sup35, indicating an involvement of the yeast prion [PSI(+)]. Respiratory deficiency of MB43-nam9-1 can be reinduced by transfer of cytosol from S. cerevisiae that harbors [PSI(+)]. We conclude that nam9-1 causes respiratory deficiency only in combination with the cytosolic prion [PSI(+)], presenting the first example of a synthetic effect between cytosolic [PSI(+)] and a mutant mitochondrial protein.

Pubmed ID: 10982839

Authors

  • Chacinska A
  • Boguta M
  • Krzewska J
  • Rospert S

Journal

Molecular and cellular biology

Publication Data

October 19, 2000

Associated Grants

None

Mesh Terms

  • Cytosol
  • DNA, Fungal
  • DNA, Mitochondrial
  • Electron Transport Complex IV
  • Fungal Proteins
  • Gene Deletion
  • Guanidine
  • Heat-Shock Proteins
  • Mitochondria
  • Nuclear Proteins
  • Oxygen Consumption
  • Peptide Termination Factors
  • Phenotype
  • Plant Proteins
  • Point Mutation
  • Prions
  • Protein Biosynthesis
  • Repressor Proteins
  • Ribosomal Proteins
  • Saccharomyces cerevisiae
  • Saccharomyces cerevisiae Proteins