MTO1 codes for a mitochondrial protein required for respiration in paromomycin-resistant mutants of Saccharomyces cerevisiae.
Mutations in MTO1 express a respiratory defect only in the context of a mitochondrial genome with a paromomycin-resistance allele. This phenotype is similar to that described previously for mss1 mutants by Decoster, E., Vassal, A., and Faye, G. (1993) J. Mol. Biol. 232, 79-88. We present evidence that Mto1p and Mss1p are mitochondrial proteins and that they form a heterodimer complex. In a paromomycin-resistant background, mss1 and mto1 mutants are inefficient in processing the mitochondrial COX1 transcript for subunit 1 of cytochrome oxidase. The mutants also fail to synthesize subunit 1 and show a pleiotropic absence of cytochromes a, a3, and b. In vivo pulse labeling of an mto1 mutant, however, indicate increased rates of synthesis of other mitochondrial translation products. The respiratory defective phenotype of mto1 and mss1 mutants is not seen in a paromomycin-sensitive genetic background. The visible absorption spectra of such strains indicate a higher ratio of cytochromes b/a and elevated NADH- and succinate-cytochrome c reductase activities. To explain these phenotypic characteristics, we proposed that the Mto1p.Mss1p complex plays a role in optimizing mitochondrial protein synthesis in yeast, possibly by a proofreading mechanism.
Colby
G
G
Department of Biological Sciences, Columbia University, New York, New York 10027, USA.
Wu
M
M
Tzagoloff
A
A
D000900:Anti-Bacterial Agents / Q000494:pharmacology; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism*; D002451:Cell Compartmentation; D003001:Cloning, Molecular; D017936:Cytochrome a Group / Q000032:analysis; D003573:Cytochrome b Group / Q000032:analysis; D004272:DNA, Mitochondrial / Q000235:genetics; D004352:Drug Resistance, Microbial; D004579:Electron Transport; D003576:Electron Transport Complex IV / Q000235:genetics; D020558:GTP Phosphohydrolases / Q000235:genetics; D019204:GTP-Binding Proteins; D005800:Genes, Fungal; D005816:Genetic Complementation Test; D008928:Mitochondria / Q000187:drug effects / Q000235:genetics*; D024101:Mitochondrial Proteins; D009245:NADH Dehydrogenase / Q000032:analysis; D010101:Oxygen Consumption / Q000235:genetics*; D010303:Paromomycin / Q000494:pharmacology*; D010641:Phenotype; D011485:Protein Binding; D012323:RNA Processing, Post-Transcriptional; D016601:RNA-Binding Proteins; D012441:Saccharomyces cerevisiae / Q000187:drug effects / Q000235:genetics*; D029701:Saccharomyces cerevisiae Proteins; D017422:Sequence Analysis, DNA; D013384:Succinate Cytochrome c Oxidoreductase / Q000032:analysis
D000900:Anti-Bacterial Agents; D002352:Carrier Proteins; D017936:Cytochrome a Group; D003573:Cytochrome b Group; D004272:DNA, Mitochondrial; C115189:MTO1 protein, S cerevisiae; D024101:Mitochondrial Proteins; D016601:RNA-Binding Proteins; D029701:Saccharomyces cerevisiae Proteins; D010303:Paromomycin; D013384:Succinate Cytochrome c Oxidoreductase; D009245:NADH Dehydrogenase; D003576:Electron Transport Complex IV; D020558:GTP Phosphohydrolases; D019204:GTP-Binding Proteins; C082241:MSS1 protein, S cerevisiae