Yasukawa T, Hino N, Suzuki T, Watanabe K, Ueda T, Ohta S
Department of Chemistry and Biotechnology, Graduate School of Engineering, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8656, Japan.
Nucleic Acids Res. 2000 Oct 1;28(19):3779-84. doi: 10.1093/nar/28.19.3779.
Point mutations in mitochondrial tRNA genes are responsible for individual subgroups of mitochondrial encephalomyopathies. We have recently reported that point mutations in the tRNA(Leu)(UUR) and tRNA(Lys) genes cause a defect in the normal modification at the first nucleotide of the anticodon. As part of a systematic analysis of pathogenic mutant mitochondrial tRNAs, we purified tRNA(Ile) with a point mutation at nucleotide 4269 to determine its nucleotide sequence, including modified nucleotides. We found that, instead of causing a defect in the post-transcriptional modification, a pathogenic point mutation in the mitochondrial tRNA(Ile) reduced the stability of the mutant tRNA molecule, resulting in a low steady-state level of aminoacyl-tRNA. The reduced stability was confirmed by examining the life-span of the mutant tRNA(Ile) both in vitro and in vivo, as well as by monitoring its melting profile. Our finding indicates that the mutant tRNA(Ile) itself is intrinsically unstable.
线粒体tRNA基因中的点突变是线粒体脑肌病各个亚组的病因。我们最近报道,tRNA(Leu)(UUR)和tRNA(Lys)基因中的点突变会导致反密码子第一位核苷酸正常修饰的缺陷。作为对致病性突变线粒体tRNA进行系统分析的一部分,我们纯化了在核苷酸4269处存在点突变的tRNA(Ile),以确定其核苷酸序列,包括修饰核苷酸。我们发现,线粒体tRNA(Ile)中的致病性点突变并没有导致转录后修饰缺陷,而是降低了突变tRNA分子的稳定性,导致氨酰-tRNA的稳态水平较低。通过在体外和体内检测突变tRNA(Ile)的寿命以及监测其解链曲线,证实了其稳定性降低。我们的发现表明,突变tRNA(Ile)本身本质上是不稳定的。