ArticleEMBO reports2003
The yeast counterparts of human 'MELAS' mutations cause mitochondrial dysfunction that can be rescued by overexpression of the mitochondrial translation factor EF-Tu.
Article in EMBO reports, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 66 citations in OpenAlex.
- Preclinical models of mitochondrial dysfunction: mtDNA and nuclear-encoded regulators in diverse pathologies.Frontiers in aging · 2025Review
- Molecular basis of diseases induced by the mitochondrial DNA mutation m.9032T>C.Human molecular genetics · 2023Article
- Leigh Syndrome: A Tale of Two Genomes.Frontiers in physiology · 2021Review
- Statins interfere with the attachment ofJournal of enzyme inhibition and medicinal chemistry · 2020Article
- Perspective on AMD Pathobiology: A Bioenergetic Crisis in the RPE.Investigative ophthalmology & visual science · 2018Review
- Yeast as a system for modeling mitochondrial disease mechanisms and discovering therapies.Disease models & mechanisms · 2015Review
- Article
- The phenotypic expression of mitochondrial tRNA-mutations can be modulated by either mitochondrial leucyl-tRNA synthetase or the C-terminal domain thereof.Frontiers in genetics · 2015Article
- Strain-specific nuclear genetic background differentially affects mitochondria-related phenotypes in Saccharomyces cerevisiae.MicrobiologyOpen · 2014Article
- Human mitochondrial leucyl tRNA synthetase can suppress non cognate pathogenic mt-tRNA mutations.EMBO molecular medicine · 2014Article
- Human mitochondrial disease-like symptoms caused by a reduced tRNA aminoacylation activity in flies.Nucleic acids research · 2013Article
- Intrinsic apoptotic pathway and G2/M cell cycle arrest involved in tubeimoside I-induced EC109 cell death.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2013Article
- 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
- Peptides from aminoacyl-tRNA synthetases can cure the defects due to mutations in mt tRNA genes.Mitochondrion · 2011Article
- Structural and functional role of bases 32 and 33 in the anticodon loop of yeast mitochondrial tRNAIle.RNA (New York, N.Y.) · 2011Article
- Correction of the consequences of mitochondrial 3243A>G mutation in the MT-TL1 gene causing the MELAS syndrome by tRNA import into mitochondria.Nucleic acids research · 2011Article
- Human mitochondrial leucyl-tRNA synthetase corrects mitochondrial dysfunctions due to the tRNALeu(UUR) A3243G mutation, associated with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like symptoms and diabetes.Molecular and cellular biology · 2010Article
- Evaluation of the mitochondrial respiratory chain and oxidative phosphorylation system using yeast models of OXPHOS deficiencies.Current protocols in human genetics · 2009Article
- Overexpressed mitochondrial leucyl-tRNA synthetase suppresses the A3243G mutation in the mitochondrial tRNA(Leu(UUR)) gene.RNA (New York, N.Y.) · 2008Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have taken advantage of the similarity between human and yeast (Saccharomyces cerevisiae) mitochondrial tRNA(Leu)(UUR), and of the possibility of transforming yeast mitochondria, to construct yeast mitochondrial mutations in the gene encoding tRNA(Leu)(UUR) equivalent to the human A3243G, C3256T and T3291C mutations that have been found in patients with the neurodegenerative disease MELAS (for mitochondrial 'myopathy, encephalopathy, lactic acidosis and stroke-like episodes'). The resulting yeast cells (bearing the equivalent mutations A14G, C26T and T69C) were defective for growth on respiratory substrates, exhibited an abnormal mitochondrial morphology, and accumulated mitochondrial DNA deletions at a very high rate, a trait characteristic of severe mitochondrial defects in protein synthesis. This effect was specific at least in the pathogenic mutation T69C, because when we introduced A or G instead of C, the respiratory defect was absent or very mild. All defective phenotypes returned to normal when the mutant cells were transformed by multicopy plasmids carrying the gene encoding the mitochondrial elongation factor EF-Tu. The ability to create and analyse such mutated strains and to select correcting genes should make yeast a good model for the study of tRNAs and their interacting partners and a practical tool for the study of pathological mutations and of tRNA sequence polymorphisms.
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