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tRNA反密码子摆动位置上C5尿苷修饰的解码特性。

Decoding property of C5 uridine modification at the wobble position of tRNA anticodon.

作者信息

Kurata Shinya, Ohtsuki Takashi, Wada Takeshi, Kirino Yohei, Takai Kazuyuki, Saigo Kazuhiko, Watanabe Kimitsuna, Suzuki Tsutomu

机构信息

Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, Bldg. FSB-301, 5-1-5 Kashiwanoha, Kashiwa, Chiba Prefecture, 277-8562, Japan.

出版信息

Nucleic Acids Res Suppl. 2003(3):245-6. doi: 10.1093/nass/3.1.245.

DOI:10.1093/nass/3.1.245
PMID:14510472
Abstract

Post-transcriptional modification at the first (wobble) position of the tRNA anticodon participates in precise decoding of the genetic code. We recently identified a novel taurine-containing modified uridine (tau m5U; 5-taurinomethyluridine) at the wobble position of mammalian mitochondrial tRNAs and found lack of this modification in mutant mitochondrial tRNAs from human pathogenic cells of the mitochondrial encephalomyopathies, investigate molecular pathogenesis of the diseases, decoding activity of wobble uridines with or without C5 modification was measured using E. coli cell-free translation system. It has been revealed that C5 modification has a functional role for stabilizing U:G wobble base pair.

摘要

转运RNA(tRNA)反密码子第一位(摆动位)的转录后修饰参与遗传密码的精确解码。我们最近在哺乳动物线粒体tRNA的摆动位鉴定出一种新型的含牛磺酸的修饰尿苷(tau m5U;5-牛磺甲基尿苷),并发现来自线粒体脑肌病患者致病细胞的突变线粒体tRNA中缺乏这种修饰。为研究这些疾病的分子发病机制,我们使用大肠杆菌无细胞翻译系统测量了具有或不具有C5修饰的摆动尿苷的解码活性。结果表明,C5修饰对于稳定U:G摆动碱基对具有功能性作用。

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Decoding property of C5 uridine modification at the wobble position of tRNA anticodon.tRNA反密码子摆动位置上C5尿苷修饰的解码特性。
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Modified uridines with C5-methylene substituents at the first position of the tRNA anticodon stabilize U.G wobble pairing during decoding.在tRNA反密码子第一位带有C5-亚甲基取代基的修饰尿苷在解码过程中稳定U.G摆动配对。
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A single uridine modification at the wobble position of an artificial tRNA enhances wobbling in an Escherichia coli cell-free translation system.人工tRNA摆动位置的单个尿苷修饰增强了大肠杆菌无细胞翻译系统中的摆动。
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Nutrients. 2017 Jul 25;9(8):795. doi: 10.3390/nu9080795.
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MTO1 mediates tissue specificity of OXPHOS defects via tRNA modification and translation optimization, which can be bypassed by dietary intervention.MTO1通过tRNA修饰和翻译优化介导氧化磷酸化缺陷的组织特异性,而饮食干预可绕过这一过程。
Hum Mol Genet. 2015 Apr 15;24(8):2247-66. doi: 10.1093/hmg/ddu743. Epub 2014 Dec 30.