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线粒体DNA的多处缺失会去除轻链复制起点。

Multiple deletions of mtDNA remove the light strand origin of replication.

作者信息

Bank C, Soulimane T, Schröder J M, Buse G, Zanssen S

机构信息

Institut für Biochemie, Institut für Neuropathologie, Pauwelsstrasse 30, Aachen, D-52074, Germany.

出版信息

Biochem Biophys Res Commun. 2000 Dec 20;279(2):595-601. doi: 10.1006/bbrc.2000.3951.

Abstract

Idiopathic inflammatory myopathies are progressive, debilitating muscle diseases. The pathogenesis of these disorders is multifactorial and appears to include mutations of the mitochondrial genome, which are usually indicated by morphological changes of mitochondria. The vast majority of all mitochondrial DNA deletions found are located between the origins of replication in the "major region" between nt5760-nt190. Using long distance PCR and sequencing techniques, we detected deletions which were unusually large (ca. 10500-12800 bp) and show uncommon 5'-breakpoints between nt800 and nt3326. Unlike most other deletions, their breakpoints are far upstream of the "major region." The atypical location of these deletions suggests a different pathomechanism. The impact of the mitochondrial DNA deletions in the pathogenetic cascade remains uncertain.

摘要

特发性炎性肌病是进行性、使人衰弱的肌肉疾病。这些疾病的发病机制是多因素的,似乎包括线粒体基因组的突变,线粒体的形态变化通常表明存在这种突变。发现的所有线粒体DNA缺失绝大多数位于nt5760 - nt190之间“主要区域”的复制起点之间。使用长距离PCR和测序技术,我们检测到异常大的缺失(约10500 - 12800 bp),并在nt800和nt3326之间显示出不常见的5'断点。与大多数其他缺失不同,它们的断点在“主要区域”的上游很远。这些缺失的非典型位置提示了一种不同的发病机制。线粒体DNA缺失在发病机制级联反应中的影响仍不确定。

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