Generation of trans-mitochondrial mito-mice by the introduction of a pathogenic G13997A mtDNA from highly metastatic lung carcinoma cells
Generation of trans-mitochondrial mito-mice by the introduction of a pathogenic G13997A mtDNA from highly metastatic lung carcinoma cells
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DOI：
10.1016/j.febslet.2010.07.048
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发表时间：
2010-09-24
期刊：
影响因子：
3.5
通讯作者：
Hayashi, Jun-Ichi
中科院分区：
文献类型：
--
作者：
Yokota, Mutsumi;Shitara, Hiroshi;Hayashi, Jun-Ichi
为了研究呼吸缺陷对疾病表型的影响，我们通过引入突变的G13997A线粒体DNA，特异性地诱导小鼠肿瘤细胞的呼吸复合体I缺陷和转移潜能，产生了跨线粒体小鼠(有丝分裂小鼠)。首先，我们获得了含有G13997A线粒体DNA的ES细胞和嵌合小鼠，然后我们通过其雌性生殖系传递产生了携带G13997A线粒体DNA的有丝分裂小鼠。三个月大的有丝分裂小鼠表现出复杂的i缺陷和乳酸过量生产，但没有表现出与线粒体疾病或肿瘤形成有关的其他表型，这表明其他表型的表达需要衰老或额外的核异常。(C)2010年欧洲生化学会联合会。爱思唯尔出版，版权所有。
To investigate the effects of respiration defects on the disease phenotypes, we generated trans-mitochondrial mice (mito-mice) by introducing a mutated G13997A mtDNA, which specifically induces respiratory complex I defects and metastatic potentials in mouse tumor cells. First, we obtained ES cells and chimeric mice containing the G13997A mtDNA, and then we generated mito-mice carrying the G13997A mtDNA via its female germ line transmission. The three-month-old mito-mice showed complex I defects and lactate overproduction, but showed no other phenotypes related to mitochondrial diseases or tumor formation, suggesting that aging or additional nuclear abnormalities are required for expression of other phenotypes. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.