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

Bongki Cho, Hyo Min Cho, Youhwa Jo, Hee Dae Kim, Myungjae Song, Cheil Moon, Hyongbum Kim, Kyungjin Kim, Hiromi Sesaki, Im Joo Rhyu, Hyun Kim and Woong Sun ()
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Bongki Cho: Korea University College of Medicine
Hyo Min Cho: Korea University College of Medicine
Youhwa Jo: Korea University College of Medicine
Hee Dae Kim: Seoul National University
Myungjae Song: Yonsei University College of Medicine
Cheil Moon: Daegu Gyeongbuk Institute of Science and Technology
Hyongbum Kim: Yonsei University College of Medicine
Kyungjin Kim: Daegu Gyeongbuk Institute of Science and Technology
Hiromi Sesaki: Johns Hopkins University School of Medicine
Im Joo Rhyu: Korea University College of Medicine
Hyun Kim: Korea University College of Medicine
Woong Sun: Korea University College of Medicine

Nature Communications, 2017, vol. 8, issue 1, 1-17

Abstract: Abstract 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.

Date: 2017
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DOI: 10.1038/ncomms15754

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