ArticleNucleic acids research2018
A natural non-Watson-Crick base pair in human mitochondrial tRNAThr causes structural and functional susceptibility to local mutations.
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 21 papers.
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21 citing papers in PubMed.
- Anticodon loop remodeling and D-stem shape drive the specific recognition of ANN-decoding tRNAs for t6A modification.Nucleic acids research · 2026Article
- Structures of KEOPS bound to tRNA reveal functional roles of the kinase Bud32.Nature communications · 2024Article
- Taurine hypomodification underlies mitochondrial tRNATrp-related genetic diseases.Nucleic acids research · 2024Article
- tRNA Modifications and Dysregulation: Implications for Brain Diseases.Brain sciences · 2024Review
- Multifaceted roles of t6A biogenesis in efficiency and fidelity of mitochondrial gene expression.Nucleic acids research · 2024Article
- Conservation and Diversification of tRNA tInternational journal of molecular sciences · 2022Review
- Toxic and nutritional factors trigger Leber hereditary optic neuropathy due to a mitochondrial tRNA mutation.Clinical genetics · 2022Article
- Molecular basis for human mitochondrial tRNA m3C modification by alternatively spliced METTL8.Nucleic acids research · 2022Article
- Structural basis for impaired 5' processing of a mutant tRNA associated with defects in neuronal homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Commonality and diversity in tRNA substrate recognition in t6A biogenesis by eukaryotic KEOPSs.Nucleic acids research · 2022Article
- The structural and functional workings of KEOPS.Nucleic acids research · 2021Review
- Disease-associated mutations in mitochondrial precursor tRNAs affect binding, m1R9 methylation, and tRNA processing by mtRNase P.RNA (New York, N.Y.) · 2021Article
- The human tRNA taurine modification enzyme GTPBP3 is an active GTPase linked to mitochondrial diseases.Nucleic acids research · 2021Article
- Nitrosative stress inhibits aminoacylation and editing activities of mitochondrial threonyl-tRNA synthetase by S-nitrosation.Nucleic acids research · 2020Article
- Screening for deafness-associated mitochondrial 12S rRNA mutations by using a multiplex allele-specific PCR method.Bioscience reports · 2020Article
- Molecular basis for t6A modification in human mitochondria.Nucleic acids research · 2020Article
- Role of Wybutosine and MgACS omega · 2019Article
- Frequency and spectrum ofMitochondrial DNA. Part B, Resources · 2019Article
- The G3-U70-independent tRNA recognition by human mitochondrial alanyl-tRNA synthetase.Nucleic acids research · 2019Article
- A coronary artery disease-associated tRNAThr mutation altered mitochondrial function, apoptosis and angiogenesis.Nucleic acids research · 2019Article
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6 authors.
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Abstract
Six pathogenic mutations have been reported in human mitochondrial tRNAThr (hmtRNAThr); however, the pathogenic molecular mechanism remains unclear. Previously, we established an activity assay system for human mitochondrial threonyl-tRNA synthetase (hmThrRS). In the present study, we surveyed the structural and enzymatic effects of pathogenic mutations in hmtRNAThr and then focused on m.15915 G > A (G30A) and m.15923A > G (A38G). The harmful evolutionary gain of non-Watson-Crick base pair A29/C41 caused hmtRNAThr to be highly susceptible to mutations disrupting the G30-C40 base pair in various ways; for example, structural integrity maintenance, modification and aminoacylation of tRNAThr, and editing mischarged tRNAThr. A similar phenomenon was observed for hmtRNATrp with an A29/C41 non-Watson-Crick base pair, but not in bovine mtRNAThr with a natural G29-C41 base pair. The A38G mutation caused a severe reduction in Thr-acceptance and editing of hmThrRS. Importantly, A38 is a nucleotide determinant for the t6A modification at A37, which is essential for the coding properties of hmtRNAThr. In summary, our results revealed the crucial role of the G30-C40 base pair in maintaining the proper structure and function of hmtRNAThr because of A29/C41 non-Watson-Crick base pair and explained the molecular outcome of pathogenic G30A and A38G mutations.
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