Xenomitochondrial mice: Investigation into mitochondrial compensatory mechanisms
Xenomitochondrial mice: Investigation into mitochondrial compensatory mechanisms
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DOI：
10.1016/j.mito.2010.07.003
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发表时间：
2011-01-01
期刊：
影响因子：
4.4
通讯作者：
Pinkert, C. A.
中科院分区：
文献类型：
--
作者：
Cannon, M. V.;Dunn, D. A.;Pinkert, C. A.
异种线粒体小鼠，在小家鼠核背景上具有进化上不同的陆地小鼠线粒体DNA（mtDNA）（B6 NTac（129 S6）-mt（M. terricolor）/Capt;品系D 7）进行分子和表型分析。与体外异种线粒体胞质杂交体研究相比，未发现明显的体内表型。微阵列分析揭示了异种线粒体小鼠中差异表达的基因，尽管没有一个直接参与线粒体功能。qRT-PCR显示在异种线粒体小鼠中mt-Co2上调。这些结果表明，轻度线粒体功能障碍的细胞代偿机制在蛋白质组学和/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。(C)2010 Elsevier B. V.和线粒体研究学会。All rights reserved.
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. (C) 2010 Elsevier B.V. and Mitochondria Research Society. All rights reserved.