Department of Pathobiology, College of Veterinary Medicine, Auburn University, Alabama 36849, United States.
Mitochondrion. 2011 Jan;11(1):33-9. doi: 10.1016/j.mito.2010.07.003. Epub 2010 Jul 16.
Xenomitochondrial mice, harboring evolutionarily divergent Mus terricolor mitochondrial DNA (mtDNA) on a Mus musculus domesticus nuclear background (B6NTac(129S6)-mt(M. terricolor)/Capt; line D7), were subjected to molecular and phenotypic analyses. No overt in vivo phenotype was identified in contrast to in vitro xenomitochondrial cybrid studies. Microarray analyses revealed differentially expressed genes in xenomitochondrial mice, though none were directly involved in mitochondrial function. qRT-PCR revealed upregulation of mt-Co2 in xenomitochondrial mice. These results illustrate that cellular compensatory mechanisms for mild mitochondrial dysfunction alter mtDNA gene expression at a proteomic and/or translational level. Understanding these mechanisms will facilitate the development of therapeutics for mitochondrial disorders.
携带在一个 Mus musculus domesticus 核背景上进化上不同的 Mus terricolor 线粒体 DNA (mtDNA) 的异源线粒体小鼠（B6NTac(129S6)-mt(M. terricolor)/Capt; 品系 D7）进行了分子和表型分析。与体外异源线粒体杂种研究相反，没有发现明显的体内表型。微阵列分析显示异源线粒体小鼠中差异表达的基因，尽管没有一个直接涉及线粒体功能。qRT-PCR 显示异源线粒体小鼠中 mt-Co2 的上调。这些结果表明，对于轻度线粒体功能障碍的细胞补偿机制会在蛋白质组学和/或翻译水平上改变 mtDNA 基因表达。了解这些机制将有助于开发线粒体疾病的治疗方法。
