CHCHD10 mutations promote loss of mitochondrial cristae junctions with impaired mitochondrial genome maintenance and inhibition of apoptosis

Abstract CHCHD10‐related diseases include mitochondrial DNA instability disorder, frontotemporal dementia‐amyotrophic lateral sclerosis (FTD‐ALS) clinical spectrum, late‐onset spinal motor neuropathy (SMAJ), and Charcot–Marie–Tooth disease type 2 (CMT2). Here, we show that CHCHD10 resides with mitof...

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Main Authors: Emmanuelle C Genin, Morgane Plutino, Sylvie Bannwarth, Elodie Villa, Eugenia Cisneros‐Barroso, Madhuparna Roy, Bernardo Ortega‐Vila, Konstantina Fragaki, Françoise Lespinasse, Estefania Pinero‐Martos, Gaëlle Augé, David Moore, Florence Burté, Sandra Lacas‐Gervais, Yusuke Kageyama, Kie Itoh, Patrick Yu‐Wai‐Man, Hiromi Sesaki, Jean‐Ehrland Ricci, Cristofol Vives‐Bauza, Véronique Paquis‐Flucklinger
Format: Article
Language:English
Published: Springer Nature 2015-12-01
Series:EMBO Molecular Medicine
Subjects:
Online Access:https://doi.org/10.15252/emmm.201505496
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author Emmanuelle C Genin
Morgane Plutino
Sylvie Bannwarth
Elodie Villa
Eugenia Cisneros‐Barroso
Madhuparna Roy
Bernardo Ortega‐Vila
Konstantina Fragaki
Françoise Lespinasse
Estefania Pinero‐Martos
Gaëlle Augé
David Moore
Florence Burté
Sandra Lacas‐Gervais
Yusuke Kageyama
Kie Itoh
Patrick Yu‐Wai‐Man
Hiromi Sesaki
Jean‐Ehrland Ricci
Cristofol Vives‐Bauza
Véronique Paquis‐Flucklinger
author_facet Emmanuelle C Genin
Morgane Plutino
Sylvie Bannwarth
Elodie Villa
Eugenia Cisneros‐Barroso
Madhuparna Roy
Bernardo Ortega‐Vila
Konstantina Fragaki
Françoise Lespinasse
Estefania Pinero‐Martos
Gaëlle Augé
David Moore
Florence Burté
Sandra Lacas‐Gervais
Yusuke Kageyama
Kie Itoh
Patrick Yu‐Wai‐Man
Hiromi Sesaki
Jean‐Ehrland Ricci
Cristofol Vives‐Bauza
Véronique Paquis‐Flucklinger
author_sort Emmanuelle C Genin
collection DOAJ
description Abstract CHCHD10‐related diseases include mitochondrial DNA instability disorder, frontotemporal dementia‐amyotrophic lateral sclerosis (FTD‐ALS) clinical spectrum, late‐onset spinal motor neuropathy (SMAJ), and Charcot–Marie–Tooth disease type 2 (CMT2). Here, we show that CHCHD10 resides with mitofilin, CHCHD3 and CHCHD6 within the “mitochondrial contact site and cristae organizing system” (MICOS) complex. CHCHD10 mutations lead to MICOS complex disassembly and loss of mitochondrial cristae with a decrease in nucleoid number and nucleoid disorganization. Repair of the mitochondrial genome after oxidative stress is impaired in CHCHD10 mutant fibroblasts and this likely explains the accumulation of deleted mtDNA molecules in patient muscle. CHCHD10 mutant fibroblasts are not defective in the delivery of mitochondria to lysosomes suggesting that impaired mitophagy does not contribute to mtDNA instability. Interestingly, the expression of CHCHD10 mutant alleles inhibits apoptosis by preventing cytochrome c release.
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spelling doaj-art-a6eda45384124c2da28b788438fcf63d2025-08-20T03:46:16ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842015-12-0181587210.15252/emmm.201505496CHCHD10 mutations promote loss of mitochondrial cristae junctions with impaired mitochondrial genome maintenance and inhibition of apoptosisEmmanuelle C Genin0Morgane Plutino1Sylvie Bannwarth2Elodie Villa3Eugenia Cisneros‐Barroso4Madhuparna Roy5Bernardo Ortega‐Vila6Konstantina Fragaki7Françoise Lespinasse8Estefania Pinero‐Martos9Gaëlle Augé10David Moore11Florence Burté12Sandra Lacas‐Gervais13Yusuke Kageyama14Kie Itoh15Patrick Yu‐Wai‐Man16Hiromi Sesaki17Jean‐Ehrland Ricci18Cristofol Vives‐Bauza19Véronique Paquis‐Flucklinger20IRCAN, UMR CNRS 7284/INSERM U1081/UNS, School of Medicine, Nice Sophia‐Antipolis UniversityIRCAN, UMR CNRS 7284/INSERM U1081/UNS, School of Medicine, Nice Sophia‐Antipolis UniversityIRCAN, UMR CNRS 7284/INSERM U1081/UNS, School of Medicine, Nice Sophia‐Antipolis UniversityINSERM U1065, Centre Méditerranéen de Médecine Moléculaire (C3M), équipe “contrôle métabolique des morts cellulaires”, Nice Sophia‐Antipolis UniversityResearch Health Institute of Palma (IdISPa), Research Unit, Son Espases University HospitalDepartment of Cell Biology, Johns Hopkins University School of MedicineResearch Health Institute of Palma (IdISPa), Research Unit, Son Espases University HospitalIRCAN, UMR CNRS 7284/INSERM U1081/UNS, School of Medicine, Nice Sophia‐Antipolis UniversityIRCAN, UMR CNRS 7284/INSERM U1081/UNS, School of Medicine, Nice Sophia‐Antipolis UniversityResearch Health Institute of Palma (IdISPa), Research Unit, Son Espases University HospitalIRCAN, UMR CNRS 7284/INSERM U1081/UNS, School of Medicine, Nice Sophia‐Antipolis UniversityWellcome Trust Centre for Mitochondrial Research, Institute of Genetic Medicine, International Centre for Life, Newcastle UniversityWellcome Trust Centre for Mitochondrial Research, Institute of Genetic Medicine, International Centre for Life, Newcastle UniversityJoint Center for Applied Electron Microscopy, Nice Sophia‐Antipolis UniversityDepartment of Cell Biology, Johns Hopkins University School of MedicineDepartment of Cell Biology, Johns Hopkins University School of MedicineWellcome Trust Centre for Mitochondrial Research, Institute of Genetic Medicine, International Centre for Life, Newcastle UniversityDepartment of Cell Biology, Johns Hopkins University School of MedicineINSERM U1065, Centre Méditerranéen de Médecine Moléculaire (C3M), équipe “contrôle métabolique des morts cellulaires”, Nice Sophia‐Antipolis UniversityResearch Health Institute of Palma (IdISPa), Research Unit, Son Espases University HospitalIRCAN, UMR CNRS 7284/INSERM U1081/UNS, School of Medicine, Nice Sophia‐Antipolis UniversityAbstract CHCHD10‐related diseases include mitochondrial DNA instability disorder, frontotemporal dementia‐amyotrophic lateral sclerosis (FTD‐ALS) clinical spectrum, late‐onset spinal motor neuropathy (SMAJ), and Charcot–Marie–Tooth disease type 2 (CMT2). Here, we show that CHCHD10 resides with mitofilin, CHCHD3 and CHCHD6 within the “mitochondrial contact site and cristae organizing system” (MICOS) complex. CHCHD10 mutations lead to MICOS complex disassembly and loss of mitochondrial cristae with a decrease in nucleoid number and nucleoid disorganization. Repair of the mitochondrial genome after oxidative stress is impaired in CHCHD10 mutant fibroblasts and this likely explains the accumulation of deleted mtDNA molecules in patient muscle. CHCHD10 mutant fibroblasts are not defective in the delivery of mitochondria to lysosomes suggesting that impaired mitophagy does not contribute to mtDNA instability. Interestingly, the expression of CHCHD10 mutant alleles inhibits apoptosis by preventing cytochrome c release.https://doi.org/10.15252/emmm.201505496CHCHD10mitochondriamitochondrial diseasemotor neuron diseasemtDNA instability
spellingShingle Emmanuelle C Genin
Morgane Plutino
Sylvie Bannwarth
Elodie Villa
Eugenia Cisneros‐Barroso
Madhuparna Roy
Bernardo Ortega‐Vila
Konstantina Fragaki
Françoise Lespinasse
Estefania Pinero‐Martos
Gaëlle Augé
David Moore
Florence Burté
Sandra Lacas‐Gervais
Yusuke Kageyama
Kie Itoh
Patrick Yu‐Wai‐Man
Hiromi Sesaki
Jean‐Ehrland Ricci
Cristofol Vives‐Bauza
Véronique Paquis‐Flucklinger
CHCHD10 mutations promote loss of mitochondrial cristae junctions with impaired mitochondrial genome maintenance and inhibition of apoptosis
EMBO Molecular Medicine
CHCHD10
mitochondria
mitochondrial disease
motor neuron disease
mtDNA instability
title CHCHD10 mutations promote loss of mitochondrial cristae junctions with impaired mitochondrial genome maintenance and inhibition of apoptosis
title_full CHCHD10 mutations promote loss of mitochondrial cristae junctions with impaired mitochondrial genome maintenance and inhibition of apoptosis
title_fullStr CHCHD10 mutations promote loss of mitochondrial cristae junctions with impaired mitochondrial genome maintenance and inhibition of apoptosis
title_full_unstemmed CHCHD10 mutations promote loss of mitochondrial cristae junctions with impaired mitochondrial genome maintenance and inhibition of apoptosis
title_short CHCHD10 mutations promote loss of mitochondrial cristae junctions with impaired mitochondrial genome maintenance and inhibition of apoptosis
title_sort chchd10 mutations promote loss of mitochondrial cristae junctions with impaired mitochondrial genome maintenance and inhibition of apoptosis
topic CHCHD10
mitochondria
mitochondrial disease
motor neuron disease
mtDNA instability
url https://doi.org/10.15252/emmm.201505496
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