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慢性进行性眼外肌麻痹与线粒体天冬酰胺tRNA基因的一种新突变相关。

Chronic progressive external ophthalmoplegia is associated with a novel mutation in the mitochondrial tRNA(Asn) gene.

作者信息

Seibel P, Lauber J, Klopstock T, Marsac C, Kadenbach B, Reichmann H

机构信息

Neurologische Universitätsklinik, Würzburg, Germany.

出版信息

Biochem Biophys Res Commun. 1994 Oct 28;204(2):482-9. doi: 10.1006/bbrc.1994.2485.

Abstract

Chronic progressive external ophthalmoplegia (CPEO) is caused by a decreased oxidative phosphorylation (OXPHOS) activity due to large-scale deletions of the mitochondrial genome in 50% of the patients. The deletions encompass structural OXPHOS genes as well as tRNA genes, required for their expression so that the pathogenesis could be due to the deleted OXPHOS subunits or to an impaired mitochondrial translation. We have analyzed the mitochondrial genome of a patient presenting with CPEO for single base substitutions and discovered a novel heteroplasmic mutation in the tRNA(Asn) gene at position 5692 that converts a highly conserved adenine into a guanine. This mutation is unique because it is located at the transition of the anticodon loop to the anticodon stem and it leads to an additional base pair, thus reducing the number of loop-forming nucleotides from seven to five. Our findings suggest that CPEO can be caused by a single base substitution in a mitochondrial tRNA gene so that the mitochondrial protein synthesis becomes the rate limiting step in OXPHOS fidelity.

摘要

慢性进行性眼外肌麻痹(CPEO)在50%的患者中是由线粒体基因组的大规模缺失导致氧化磷酸化(OXPHOS)活性降低引起的。这些缺失包括结构性OXPHOS基因以及它们表达所需的tRNA基因,因此发病机制可能是由于缺失的OXPHOS亚基或线粒体翻译受损。我们分析了一名患有CPEO患者的线粒体基因组中的单碱基替换,发现在tRNA(Asn)基因的5692位存在一个新的异质性突变,该突变将一个高度保守的腺嘌呤转换为鸟嘌呤。这个突变是独特的,因为它位于反密码子环与反密码子茎的交界处,并且导致了一个额外的碱基对,从而使形成环的核苷酸数量从七个减少到五个。我们的研究结果表明,CPEO可能由线粒体tRNA基因中的单个碱基替换引起,从而使线粒体蛋白质合成成为OXPHOS保真度的限速步骤。

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