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Nat Commun. 2017 Jun 9;8:15754. doi: 10.1038/ncomms15754.

Constriction of the mitochondrial inner compartment is a priming event for mitochondrial division.

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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.
Department of Biological Sciences, Seoul National University, Seoul 08826, Republic of Korea.
Department of Pharmacology, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemoon-gu, Seoul 03722, Republic of Korea.
Korea Brain Research Institute, 61 Choeomdan-Ro, Dong-Gu, Daegu 41068, Republic of Korea.
Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.


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 Ca2+ 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.

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