ArticleRNA (New York, N.Y.)2008
Yeast as a model of human mitochondrial tRNA base substitutions: investigation of the molecular basis of respiratory defects.
Article in RNA (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
- Peptide-mimetics derived from leucyl-tRNA synthetase are potential agents for the therapy of mt-tRNA related diseases.Frontiers in pharmacology · 2025Article
- Molecular basis of diseases induced by the mitochondrial DNA mutation m.9032T>C.Human molecular genetics · 2023Article
- The Power of Yeast in Modelling Human Nuclear Mutations Associated with Mitochondrial Diseases.Genes · 2021Review
- Leigh Syndrome: A Tale of Two Genomes.Frontiers in physiology · 2021Review
- Statins interfere with the attachment ofJournal of enzyme inhibition and medicinal chemistry · 2020Article
- Mapping and editing animal mitochondrial genomes: can we overcome the challenges?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Review
- Gcn5 histone acetyltransferase is present in the mitoplasts.Biology open · 2019Article
- Overexpression of mitochondrial oxodicarboxylate carrier (ODC1) preserves oxidative phosphorylation in a yeast model of Barth syndrome.Disease models & mechanisms · 2017Article
- Yeast as a system for modeling mitochondrial disease mechanisms and discovering therapies.Disease models & mechanisms · 2015Review
- Identification of lethal mutations in yeast threonyl-tRNA synthetase revealing critical residues in its human homolog.The Journal of biological chemistry · 2015Article
- Strain-specific nuclear genetic background differentially affects mitochondria-related phenotypes in Saccharomyces cerevisiae.MicrobiologyOpen · 2014Article
- Higher order structural effects stabilizing the reverse Watson-Crick Guanine-Cytosine base pair in functional RNAs.Nucleic acids research · 2014Article
- The power of yeast to model diseases of the powerhouse of the cell.Frontiers in bioscience (Landmark edition) · 2013Review
- Screening of effective pharmacological treatments for MELAS syndrome using yeasts, fibroblasts and cybrid models of the disease.British journal of pharmacology · 2012Article
- Structural and functional role of bases 32 and 33 in the anticodon loop of yeast mitochondrial tRNAIle.RNA (New York, N.Y.) · 2011Article
- Peptides from aminoacyl-tRNA synthetases can cure the defects due to mutations in mt tRNA genes.Mitochondrion · 2011Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
We investigate the relationships between acylation defects and structure alterations due to base substitutions in yeast mitochondrial (mt) tRNA(UUR)(Leu). The studied substitutions are equivalent to the A3243G and T3250C human pathogenetic tRNA mutations. Our data show that both mutations can produce tRNA(UUR)(Leu) acylation defects, although to a different extent. For mutant A14G (equivalent to MELAS A3243G base substitution), the presence of the tRNA and its defective aminoacylation could be observed only in the nuclear context of W303, a strain where the protein synthesis defects caused by tRNA base substitutions are far less severe than in previously studied strains. For mutant T20C (equivalent to the MM/CPEO human T3250C mutation), the acylation defect was less severe, and a thermosensitive acylation could be detected also in the MCC123 strain. The correlation between the severity of the in vivo phenotypes of yeast tRNA mutants and those obtained in in vitro studies of human tRNA mutants supports the view that yeast is a suitable model to study the cellular and molecular effects of tRNA mutations involved in human pathologies. Furthermore, the yeast model offers the possibility of modulating the severity of yeast respiratory phenotypes by studying the tRNA mutants in different nuclear contexts. The nucleotides at positions 14 and 20 are both highly conserved in yeast and human mt tRNAs; however, the different effect of their mutations can be explained by structure analyses and quantum mechanics calculations that can shed light on the molecular mechanisms responsible for the experimentally determined defects of the mutants.
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