Searching across hundreds of databases

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

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 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