Karbowski M, Spodnik J H, Teranishi M, Wozniak M, Nishizawa Y, Usukura J, Wakabayashi T
Department of Cell Biology and Molecular Pathology, Nagoya University School of Medicine, Nagoya, Japan.
J Cell Sci. 2001 Jan;114(Pt 2):281-91. doi: 10.1242/jcs.114.2.281.
Distribution of mitochondria as well as other intracellular organelles in mammalian cells is regulated by interphase microtubules. Here, we demonstrate a role of microtubules in the mitochondrial biogenesis using various microtubule-active drugs and human osteosarcoma cell line 143B cells and rat liver-derived RL-34 cells. Depolymerization of microtubules by nocodazole or colchicine, as well as 2-methoxyestradiol, a natural estrogen metabolite, arrested asynchronously cultured cells in G(2)/M phase of cell cycle and at the same time inhibited the mitochondrial mass increase and mtDNA replication. These drugs also inhibited the mitochondrial mass increase in the cells that were synchronized in cell cycle, which should occur during G(1) to G(2) phase progression in normal conditions. However, stabilization of microtubules by taxol did not affect the proliferation of mitochondria during the cell cycle, yet a prolonged incubation of cells with taxol induced an abnormal accumulation of mitochondria in cells arrested in G(2)/M phase of cell cycle. Taxol-induced accumulation of mitochondria was not only demonstrated by mitochondria-specific fluorescent dyes but also evidenced by the examination of cells transfected with yellow fluorescent protein fused with mitochondrial targeting sequence from subunit VIII of human cytochrome c oxidase (pEYFP) and by enhanced mtDNA replication. Two subpopulations of mitochondria were detected in taxol-treated cells: mitochondria with high Delta(psi)(m), detectable either by Mito Tracker Red CMXRos or by Green FM, and those with low Delta(psi)(m), detectable only by Green FM. However, taxol-induced increases in the mitochondrial mass and in the level of acetylated (alpha)-tubulin were abrogated by a co-treatment with taxol and nocodazole or taxol and colchicine. These data strongly suggest that interphase microtubules may be essential for the regulation of mitochondrial biogenesis in mammalian cells.
哺乳动物细胞中线粒体以及其他细胞内细胞器的分布受间期微管调控。在此,我们使用多种微管活性药物以及人骨肉瘤细胞系143B细胞和大鼠肝脏来源的RL - 34细胞,证明了微管在线粒体生物发生中的作用。诺考达唑或秋水仙碱使微管解聚,以及天然雌激素代谢产物2 - 甲氧基雌二醇,使异步培养的细胞停滞在细胞周期的G(2)/M期,同时抑制线粒体质量增加和线粒体DNA复制。这些药物还抑制了细胞周期同步化细胞中的线粒体质量增加,而在正常情况下,这一过程应发生在从G(1)到G(2)期的进程中。然而,紫杉醇使微管稳定化并不影响细胞周期中线粒体的增殖,但细胞用紫杉醇长时间孵育会导致停滞在细胞周期G(2)/M期的细胞中线粒体异常积累。紫杉醇诱导的线粒体积累不仅通过线粒体特异性荧光染料得以证明,还通过对转染了与人细胞色素c氧化酶亚基VIII的线粒体靶向序列融合的黄色荧光蛋白(pEYFP)的细胞进行检测以及增强的线粒体DNA复制得以证实。在紫杉醇处理的细胞中检测到两个线粒体亚群:通过Mito Tracker Red CMXRos或Green FM可检测到的具有高膜电位(Δψ(m))的线粒体,以及仅通过Green FM可检测到的具有低膜电位(Δψ(m))的线粒体。然而,紫杉醇与诺考达唑或紫杉醇与秋水仙碱共同处理可消除紫杉醇诱导的线粒体质量增加和乙酰化α - 微管水平升高。这些数据有力地表明,间期微管可能对哺乳动物细胞中线粒体生物发生的调控至关重要。