Department of Anatomy, Korea University College of Medicine, 145 Anam-ro, Seongbuk-gu, Seoul 02841, Republic of Korea.
Department of Brain &Cognitive Sciences, Daegu Gyeongbuk Institute of Science and Technology, 333 Techno Jungang-daero, Hyeonpung-myeon, Dalseong-gun, Daegu 42988, Republic of Korea.
Nat Commun. 2017 Jun 9;8:15754. doi: 10.1038/ncomms15754.
Mitochondrial division is critical for the maintenance and regulation of mitochondrial function, quality and distribution. This process is controlled by cytosolic actin-based constriction machinery and dynamin-related protein 1 (Drp1) on mitochondrial outer membrane (OMM). Although mitochondrial physiology, including oxidative phosphorylation, is also important for efficient mitochondrial division, morphological alterations of the mitochondrial inner-membrane (IMM) have not been clearly elucidated. Here we report spontaneous and repetitive constriction of mitochondrial inner compartment (CoMIC) associated with subsequent division in neurons. Although CoMIC is potentiated by inhibition of Drp1 and occurs at the potential division spots contacting the endoplasmic reticulum, it appears on IMM independently of OMM. Intra-mitochondrial influx of Ca induces and potentiates CoMIC, and leads to K-mediated mitochondrial bulging and depolarization. Synergistically, optic atrophy 1 (Opa1) also regulates CoMIC via controlling Mic60-mediated OMM-IMM tethering. Therefore, we propose that CoMIC is a priming event for efficient mitochondrial division.
线粒体分裂对于维持和调节线粒体的功能、质量和分布至关重要。这个过程由细胞质中的肌动蛋白依赖的收缩机制和线粒体外膜（OMM）上的与 dynamin 相关蛋白 1（Drp1）控制。尽管线粒体生理学，包括氧化磷酸化，对于有效的线粒体分裂也很重要，但线粒体内膜（IMM）的形态改变还没有被清楚地阐明。在这里，我们报告了神经元中线粒体内部区室（CoMIC）的自发和重复收缩与随后的分裂有关。尽管 CoMIC 被 Drp1 的抑制所增强，并发生在与内质网接触的潜在分裂点，但它似乎独立于 OMM 出现在 IMM 上。Ca 的线粒体内部流入诱导并增强 CoMIC，并导致 K 介导的线粒体膨大和去极化。协同地，视神经萎缩 1（Opa1）也通过控制 Mic60 介导的 OMM-IMM 连接来调节 CoMIC。因此，我们提出 CoMIC 是有效线粒体分裂的启动事件。
