ArticleNucleic acids research2018
Editing activity for eliminating mischarged tRNAs is essential in mammalian mitochondria.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Advances in Research onGenes · 2026Review
- Mitochondrial translational control in cardiovascular diseases: from mechanisms to therapies.Redox biology · 2026Review
- PCBP1 regulates alternative splicing of AARS2 in congenital cardiomyopathy.Nature cardiovascular research · 2026Article
- The role of Alanyl-tRNA synthetase 1 lactylation in tumors and other diseases.Discover oncology · 2026Review
- Isoleucyl-tRNA synthetase 1 is essential for embryogenesis in mice.The Journal of veterinary medical science · 2026Article
- Eukaryotic AlaX provides multiple checkpoints for quality and quantity of aminoacyl-tRNAs in translation.Nucleic acids research · 2024Article
- Illuminating mitochondrial translation through mouse models.Human molecular genetics · 2024Review
- Mammalian mitochondrial translation infidelity leads to oxidative stress-induced cell cycle arrest and cardiomyopathy.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The tRNA identity landscape for aminoacylation and beyond.Nucleic acids research · 2023Review
- Our current understanding of the toxicity of altered mito-ribosomal fidelity during mitochondrial protein synthesis: What can it tell us about human disease?Frontiers in physiology · 2023Review
- Recessive aminoacyl-tRNA synthetase disorders: lessons learned fromFrontiers in neuroscience · 2023Review
- RNA granule-clustered mitochondrial aminoacyl-tRNA synthetases form multiple complexes with the potential to fine-tune tRNA aminoacylation.Nucleic acids research · 2022Article
- Defects in aminoacyl-tRNA synthetase cause partial B and T cell immunodeficiency.Cellular and molecular life sciences : CMLS · 2022Article
- The uniqueness of AlaRS and its human disease connections.RNA biology · 2021Review
- The regulatory roles of aminoacyl-tRNA synthetase in cardiovascular disease.Molecular therapy. Nucleic acids · 2021Review
- HumanThe Journal of biological chemistry · 2020Article
- Fine-Tuning of Alanyl-tRNA Synthetase Quality Control Alleviates Global Dysregulation of the Proteome.Genes · 2020Article
- Nitrosative stress inhibits aminoacylation and editing activities of mitochondrial threonyl-tRNA synthetase by S-nitrosation.Nucleic acids research · 2020Article
- Article
- The G3-U70-independent tRNA recognition by human mitochondrial alanyl-tRNA synthetase.Nucleic acids research · 2019Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accuracy of protein synthesis is enabled by the selection of amino acids for tRNA charging by aminoacyl-tRNA synthetases (ARSs), and further enhanced by the proofreading functions of some of these enzymes for eliminating tRNAs mischarged with noncognate amino acids. Mouse models of editing-defective cytoplasmic alanyl-tRNA synthetase (AlaRS) have previously demonstrated the importance of proofreading for cytoplasmic protein synthesis, with embryonic lethal and progressive neurodegeneration phenotypes. Mammalian mitochondria import their own set of nuclear-encoded ARSs for translating critical polypeptides of the oxidative phosphorylation system, but the importance of editing by the mitochondrial ARSs for mitochondrial proteostasis has not been known. We demonstrate here that the human mitochondrial AlaRS is capable of editing mischarged tRNAs in vitro, and that loss of the proofreading activity causes embryonic lethality in mice. These results indicate that tRNA proofreading is essential in mammalian mitochondria, and cannot be overcome by other quality control mechanisms.
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