ArticleNucleic acids research2005
A T-stem slip in human mitochondrial tRNALeu(CUN) governs its charging capacity.
Article in Nucleic acids research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 18 citations in OpenAlex.
- Maternally transmitted nonsyndromic hearing impairment may be associated with mitochondrial tRNAJournal of clinical laboratory analysis · 2022Article
- Overexpression of mitochondrial histidyl-tRNA synthetase restores mitochondrial dysfunction caused by a deafness-associated tRNAThe Journal of biological chemistry · 2020Article
- LeuRS can leucylate type I and type II tRNALeus in Streptomyces coelicolor.Nucleic acids research · 2019Article
- A natural non-Watson-Crick base pair in human mitochondrial tRNAThr causes structural and functional susceptibility to local mutations.Nucleic acids research · 2018Article
- A hypertension-associated mitochondrial DNA mutation alters the tertiary interaction and function of tRNAThe Journal of biological chemistry · 2017Article
- The Mitonuclear Dimension of Neanderthal and Denisovan Ancestry in Modern Human Genomes.Genome biology and evolution · 2017Article
- Degenerate connective polypeptide 1 (CP1) domain from human mitochondrial leucyl-tRNA synthetase.The Journal of biological chemistry · 2015Article
- A deafness-associated tRNAHis mutation alters the mitochondrial function, ROS production and membrane potential.Nucleic acids research · 2014Article
- Discovery of a potent benzoxaborole-based anti-pneumococcal agent targeting leucyl-tRNA synthetase.Scientific reports · 2013Article
- In vivo identification of essential nucleotides in tRNALeu to its functions by using a constructed yeast tRNALeu knockout strain.Nucleic acids research · 2012Article
- Accurate energies of hydrogen bonded nucleic acid base pairs and triplets in tRNA tertiary interactions.Nucleic acids research · 2006Article
- A new mechanism for mtDNA pathogenesis: impairment of post-transcriptional maturation leads to severe depletion of mitochondrial tRNASer(UCN) caused by T7512C and G7497A point mutations.Nucleic acids research · 2005Article
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human mitochondrial tRNALeu(CUN) [hmtRNALeu(CUN)] corresponds to the most abundant codon for leucine in human mitochondrial protein genes. Here, in vitro studies reveal that the U48C substitution in hmtRNALeu(CUN), which corresponds to the pathological T12311C gene mutation, improved the aminoacylation efficiency of hmtRNALeu(CUN). Enzymatic probing suggested a more flexible secondary structure in the wild-type hmtRNALeu(CUN) transcript compared with the U48C mutant. Structural analysis revealed that the flexibility of hmtRNALeu(CUN) facilitates a T-stem slip resulting in two potential tertiary structures. Several rationally designed tRNALeu(CUN) mutants were generated to examine the structural and functional consequences of the T-stem slip. Examination of these hmtRNALeu(CUN) mutants indicated that the T-stem slip governs tRNA accepting activity. These results suggest a novel, self-regulation mechanism of tRNA structure and function.
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