ArticleScientific reports2016
Aim-less translation: loss of Saccharomyces cerevisiae mitochondrial translation initiation factor mIF3/Aim23 leads to unbalanced protein synthesis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 28 citations in OpenAlex.
- Transplantation ofMicrobiology (Reading, England) · 2026Article
- Maintaining mitochondrial ribosome function: The role of ribosome rescue and recycling factors.RNA biology · 2022Review
- Yeast Mitochondrial Translation Initiation Factor 3 Interacts with Pet111p to PromoteInternational journal of molecular sciences · 2020Article
- Article
- Emerging Roles in the Biogenesis of CytochromeFrontiers in cell and developmental biology · 2019Review
- Biological and Evolutionary Significance of Terminal Extensions of Mitochondrial Translation Initiation Factor 3.International journal of molecular sciences · 2018Article
- The ribosome receptors Mrx15 and Mba1 jointly organize cotranslational insertion and protein biogenesis in mitochondria.Molecular biology of the cell · 2018Article
- Cardiomyopathy-associated mutation in the ADP/ATP carrier reveals translation-dependent regulation of cytochrome c oxidase activity.Molecular biology of the cell · 2018Article
- Proteomic profiling of the mitochondrial ribosome identifies Atp25 as a composite mitochondrial precursor protein.Molecular biology of the cell · 2016Article
- Ribosome recycling defects modify the balance between the synthesis and assembly of specific subunits of the oxidative phosphorylation complexes in yeast mitochondria.Nucleic acids research · 2016Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitochondrial genome almost exclusively encodes a handful of transmembrane constituents of the oxidative phosphorylation (OXPHOS) system. Coordinated expression of these genes ensures the correct stoichiometry of the system's components. Translation initiation in mitochondria is assisted by two general initiation factors mIF2 and mIF3, orthologues of which in bacteria are indispensible for protein synthesis and viability. mIF3 was thought to be absent in Saccharomyces cerevisiae until we recently identified mitochondrial protein Aim23 as the missing orthologue. Here we show that, surprisingly, loss of mIF3/Aim23 in S. cerevisiae does not indiscriminately abrogate mitochondrial translation but rather causes an imbalance in protein production: the rate of synthesis of the Atp9 subunit of F1F0 ATP synthase (complex V) is increased, while expression of Cox1, Cox2 and Cox3 subunits of cytochrome c oxidase (complex IV) is repressed. Our results provide one more example of deviation of mitochondrial translation from its bacterial origins.
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