Glucose starvation induces mitochondrial fragmentation depending on the dynamin GTPase Dnm1/Drp1 in fission yeast.
Glucose starvation induces mitochondrial fragmentation depending on the dynamin GTPase Dnm1/Drp1 in fission yeast.
复制标题
葡萄糖饥饿会诱导线粒体断裂，这取决于裂殖酵母中的动力 GTP 酶 Dnm1/Drp1。
DOI：
10.1074/jbc.ra119.010185
复制
发表时间：
2019
影响因子：
4.8
通讯作者：
Fu Chuanhai
中科院分区：
文献类型：
--
作者：
Zheng Fan;Jia Bowen;Dong Fenfen;Liu Ling;Rasul Faiz;He Jiajia;Fu Chuanhai
线粒体在环境胁迫下发生形态学和动力学变化。很少有研究集中在解决压力下的线粒体重塑。以裂殖酵母裂殖酵母为模型生物，研究了葡萄糖饥饿条件下线粒体的重构。我们采用活细胞显微镜监测线粒体形态和动态的细胞在充满室葡萄糖饥饿。我们的研究结果表明，在葡萄糖饥饿后几分钟内线粒体片段，并需要动力蛋白GTdom Dnm 1促进线粒体片段化。此外，我们发现，葡萄糖饥饿增强Dnm 1定位到线粒体和线粒体分裂的频率增加，但降低PKA活性。我们进一步证明，低PKA活性增强葡萄糖饥饿诱导的线粒体片段化，而高PKA活性赋予抵抗葡萄糖饥饿诱导的线粒体片段化。此外，我们观察到，AMP激活的蛋白激酶不参与调节葡萄糖饥饿下的线粒体片段化。值得注意的是，葡萄糖饥饿诱导的线粒体碎片与活性氧产生的增强有关。我们的工作提供了详细的机制的见解线粒体重塑响应葡萄糖饥饿。
Mitochondria undergo morphological and dynamic changes in response to environmental stresses. Few studies have focused on addressing mitochondrial remodeling under stress. Using the fission yeast Schizosaccharomyces pombe as a model organism, here we investigated mitochondrial remodeling under glucose starvation. We employed live-cell microscopy to monitor mitochondrial morphology and dynamics of cells in profusion chambers under glucose starvation. Our results revealed that mitochondria fragment within minutes after glucose starvation and that the dynamin GTPase Dnm1 is required for promoting mitochondrial fragmentation. Moreover, we found that glucose starvation enhances Dnm1 localization to mitochondria and increases the frequency of mitochondrial fission but decreases PKA activity. We further demonstrate that low PKA activity enhances glucose starvation–induced mitochondrial fragmentation, whereas high PKA activity confers resistance to glucose starvation–induced mitochondrial fragmentation. Moreover, we observed that AMP-activated protein kinase is not involved in regulating mitochondrial fragmentation under glucose starvation. Of note, glucose starvation–induced mitochondrial fragmentation was associated with enhanced reactive oxygen species production. Our work provides detailed mechanistic insights into mitochondrial remodeling in response to glucose starvation.