期刊
PROCEEDINGS OF THE JAPAN ACADEMY SERIES B-PHYSICAL AND BIOLOGICAL SCIENCES
卷 86, 期 1, 页码 11-39出版社
JAPAN ACAD
DOI: 10.2183/pjab.86.11
关键词
genetic code; tRNA; animal mitochondria; translation system; modified nucleotides; mitochondrial diseases
资金
- Ministry of Education, Science, Sports, and Culture of Japan
- New Energy and Industrial Technology Development Organization (NEDO)
- Human Frontier Science Program
- Grants-in-Aid for Scientific Research [21570242] Funding Source: KAKEN
In animal mitochondria, several codons are non-universal and their meanings differ depending on the species. In addition, the tRNA structures that decipher codons are sometimes unusually truncated. These features seem to be related to the shortening of mitochondrial (mt) genomes, which occurred during the evolution of mitochondria. These organelles probably originated from the endosymbiosis of an aerobic eubacterium into an ancestral enkaryote. It is plausible that these events brought about the various characteristic features of animal mt translation systems, such as genetic code variations, unusually truncated tRNA and rRNA structures, unilateral tRNA recognition mechanisms by aminoacyl-tRNA synthetases, elongation factors and ribosomes, and compensation for RNA deficits by enlarged proteins. In this article, we discuss molecular mechanisms for these phenomena. Finally, we describe human mt disease that are caused by modification defects in mt tRNAs.
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