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

http://www.ncbi.nlm.nih.gov/pubmed/10982839

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 RIS Download

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