Department of Cardiac Development and Remodelling, Max-Planck-Institute for Heart and Lung Research, Ludwigstrasse 43, 61231 Bad Nauheim, Germany.
Mitochondrion. 2011 Jul;11(4):630-4. doi: 10.1016/j.mito.2011.04.002. Epub 2011 Apr 20.
Pathological mitochondrial DNA (mtDNA) rearrangements have been proposed to result from repair of double-strand breaks caused by blockage of mitochondrial DNA (mtDNA) replication. As mtDNA deletions are seen only in post-mitotic tissues, it has been suggested that they are selected out in actively dividing cells. By electron microscopy we observed rearranged mtDNA molecules in cultured human cells expressing a catalytically impaired helicase. As these molecules were undetectable by PCR, we propose that deleted mtDNA molecules in cultured cells are fragile and sensitive to heating. Further consequences of mtDNA replication stalling are discussed.
病理性线粒体 DNA（mtDNA）重排被认为是由线粒体 DNA（mtDNA）复制受阻引起的双链断裂修复所致。由于 mtDNA 缺失仅见于有丝分裂后的组织，因此有人认为它们是在活跃分裂的细胞中被选择出来的。通过电子显微镜，我们观察到在表达催化功能受损解旋酶的培养人细胞中存在重排的 mtDNA 分子。由于这些分子通过 PCR 无法检测到，我们推测培养细胞中的缺失 mtDNA 分子是脆弱的，对加热敏感。进一步讨论了 mtDNA 复制停滞的后果。
