Fan Weiwei, Waymire Katrina G, Narula Navneet, Li Peng, Rocher Christophe, Coskun Pinar E, Vannan Mani A, Narula Jagat, Macgregor Grant R, Wallace Douglas C
Center for Molecular and Mitochondrial Medicine and Genetics, University of California, Irvine, CA 92697, USA.
Science. 2008 Feb 15;319(5865):958-62. doi: 10.1126/science.1147786.
The majority of mitochondrial DNA (mtDNA) mutations that cause human disease are mild to moderately deleterious, yet many random mtDNA mutations would be expected to be severe. To determine the fate of the more severe mtDNA mutations, we introduced mtDNAs containing two mutations that affect oxidative phosphorylation into the female mouse germ line. The severe ND6 mutation was selectively eliminated during oogenesis within four generations, whereas the milder COI mutation was retained throughout multiple generations even though the offspring consistently developed mitochondrial myopathy and cardiomyopathy. Thus, severe mtDNA mutations appear to be selectively eliminated from the female germ line, thereby minimizing their impact on population fitness.
大多数导致人类疾病的线粒体DNA(mtDNA)突变是轻度至中度有害的,但预计许多随机的mtDNA突变会更严重。为了确定更严重的mtDNA突变的命运,我们将含有两个影响氧化磷酸化的突变的mtDNA引入雌性小鼠生殖系。严重的ND6突变在四代之内的卵子发生过程中被选择性清除,而较轻的COI突变在多代中都得以保留,尽管后代持续出现线粒体肌病和心肌病。因此,严重的mtDNA突变似乎从雌性生殖系中被选择性清除,从而将它们对群体适应性的影响降至最低。