Manfredi G, Vu T, Bonilla E, Schon E A, DiMauro S, Arnaudo E, Zhang L, Rowland L P, Hirano M
H. Houston Merritt Clinical Research Center for Muscular Dystrophy and Related Disorders, and Department of Neurology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
Ann Neurol. 1997 Aug;42(2):180-8. doi: 10.1002/ana.410420208.
We identified large-scale heteroplasmic mitochondrial DNA (mtDNA) rearrangements in a 50-year-old woman with an adult-onset progressive myopathy. The predominant mtDNA abnormality was a 21.2-kb duplicated molecule. In addition, a small population of the corresponding partially deleted 4.6-kb molecule was detected. Skeletal muscle histology revealed fibers that were negative for cytochrome c oxidase (COX) activity and had reduced mtDNA-encoded COX subunits. By single-fiber polymerase chain reaction analysis, COX-negative fibers contained a low number of wild-type or duplicated mtDNA molecules (ie, nondeleted). In situ hybridization demonstrated that the abnormal fibers contained increased amounts of mtDNA compared with normal fibers and that most of the genomes were deleted. We concluded that deleted mtDNA molecules were primarily responsible for the phenotype in this patient.
我们在一名患有成人起病的进行性肌病的50岁女性中发现了大规模异质性线粒体DNA(mtDNA)重排。主要的mtDNA异常是一个21.2 kb的重复分子。此外,还检测到一小部分相应的部分缺失的4.6 kb分子。骨骼肌组织学显示,细胞色素c氧化酶(COX)活性阴性的纤维,其mtDNA编码的COX亚基减少。通过单纤维聚合酶链反应分析,COX阴性纤维中野生型或重复的mtDNA分子数量较少(即未缺失)。原位杂交表明,与正常纤维相比,异常纤维中mtDNA含量增加,且大多数基因组被删除。我们得出结论,缺失的mtDNA分子是该患者表型的主要原因。