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, Woong Sun

Research output: Contribution to journalArticle

27 Citations (Scopus)

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.

Original languageEnglish
Number of pages1
JournalNature Communications
Volume8
DOIs
Publication statusPublished - 2017 Jun 9

Fingerprint

priming
compartments
Constriction
division
constrictions
membranes
Membranes
Dynamins
Mitochondrial Membranes
Autosomal Dominant Optic Atrophy
tethering
bulging
atrophy
proteins
endoplasmic reticulum
phosphorylation
physiology
Oxidative Phosphorylation
Physiology
Depolarization

ASJC Scopus subject areas

  • Chemistry(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Physics and Astronomy(all)

Cite this

Constriction of the mitochondrial inner compartment is a priming event for mitochondrial division. / Cho, Bongki; Cho, Hyo Min; Jo, Youhwa; Kim, Hee Dae; Song, Myungjae; Moon, Cheil; Kim, Hyongbum; Kim, Kyungjin; Sesaki, Hiromi; Rhyu, Im Joo; Kim, Hyun; Sun, Woong.

In: Nature Communications, Vol. 8, 09.06.2017.

Research output: Contribution to journalArticle

Cho, Bongki ; Cho, Hyo Min ; Jo, Youhwa ; Kim, Hee Dae ; Song, Myungjae ; Moon, Cheil ; Kim, Hyongbum ; Kim, Kyungjin ; Sesaki, Hiromi ; Rhyu, Im Joo ; Kim, Hyun ; Sun, Woong. / Constriction of the mitochondrial inner compartment is a priming event for mitochondrial division. In: Nature Communications. 2017 ; Vol. 8.
@article{23966170c4344708b3affb4a5bf66dd0,
title = "Constriction of the mitochondrial inner compartment is a priming event for mitochondrial division",
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.",
author = "Bongki Cho and Cho, {Hyo Min} and Youhwa Jo and Kim, {Hee Dae} and Myungjae Song and Cheil Moon and Hyongbum Kim and Kyungjin Kim and Hiromi Sesaki and Rhyu, {Im Joo} and Hyun Kim and Woong Sun",
year = "2017",
month = "6",
day = "9",
doi = "10.1038/ncomms15754",
language = "English",
volume = "8",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "Nature Publishing Group",

}

TY - JOUR

T1 - Constriction of the mitochondrial inner compartment is a priming event for mitochondrial division

AU - Cho, Bongki

AU - Cho, Hyo Min

AU - Jo, Youhwa

AU - Kim, Hee Dae

AU - Song, Myungjae

AU - Moon, Cheil

AU - Kim, Hyongbum

AU - Kim, Kyungjin

AU - Sesaki, Hiromi

AU - Rhyu, Im Joo

AU - Kim, Hyun

AU - Sun, Woong

PY - 2017/6/9

Y1 - 2017/6/9

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=85039844400&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85039844400&partnerID=8YFLogxK

U2 - 10.1038/ncomms15754

DO - 10.1038/ncomms15754

M3 - Article

C2 - 28598422

AN - SCOPUS:85039844400

VL - 8

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

ER -