Publication:
Optic Atrophy 1 Is Epistatic to the Core MICOS Component MIC60 in Mitochondrial Cristae Shape Control

dc.contributor.authorGlytsou, Christina
dc.contributor.authorCalvo, Enrique
dc.contributor.authorCogliati, Sara
dc.contributor.authorMehrotra, Arpit
dc.contributor.authorAnastasia, Irene
dc.contributor.authorRigoni, Giovanni
dc.contributor.authorRaimondi, Andrea
dc.contributor.authorShintani, Norihito
dc.contributor.authorLoureiro, Marta
dc.contributor.authorVazquez, Jesus
dc.contributor.authorPellegrini, Luca
dc.contributor.authorEnriquez, Jose Antonio
dc.contributor.authorScorrano, Luca
dc.contributor.authorSoriano, Maria Eugenia
dc.contributor.funderTelethon Foundation (Italia)
dc.contributor.funderUnión Europea. Comisión Europea
dc.contributor.funderUnión Europea. Comisión Europea. European Research Council (ERC)
dc.contributor.funderMinistero dell Istruzione, dell Universita e della Ricerca (Italia)
dc.contributor.funderMinistero della Salute (Italia)
dc.contributor.funderUniversity of Padua (Italia)
dc.date.accessioned2017-10-20T10:33:50Z
dc.date.available2017-10-20T10:33:50Z
dc.date.issued2016
dc.description.abstractThe mitochondrial contact site and cristae organizing system (MICOS) and Optic atrophy 1 (OPA1) control cristae shape, thus affecting mitochondrial function and apoptosis. Whether and how they physically and functionally interact is unclear. Here, we provide evidence that OPA1 is epistatic to MICOS in the regulation of cristae shape. Proteomic analysis identifies multiple MICOS components in native OPA1-containing high molecular weight complexes disrupted during cristae remodeling. MIC60, a core MICOS protein, physically interacts with OPA1, and together, they control cristae junction number and stability, OPA1 being epistatic to MIC60. OPA1 defines cristae width and junction diameter independently of MIC60. Our combination of proteomics, biochemistry, genetics, and electron tomography provides a unifying model for mammalian cristae biogenesis by OPA1 and MICOS.
dc.description.peerreviewed
dc.description.sponsorshipWe thank Drs. F. Caicci and F. Boldrin (EM Facility, Department of Biology, University of Padova) for EM and ALEMBIC, San Raffaele Scientific Institute, for tomography. L.S. is a senior scientist of the Dulbecco-Telethon Institute. Support was provided by Telethon-Italy (GGP15091 and GGP14187), AIRC Italy (ERC FP7-282280), FP7 CIG (PCIG13-GA-2013-618697), the Italian Ministry of Research (FIRB RBAP11Z3YA\_005), the Italian Ministry of Health (GR-2009-1600051 to L.S.), a University of Padua grant for a postdoctoral fellowship (2015 to M.E.S.), and an International Brain Research Organization-International Society for Neurochemistry research fellowship (2016 to A.M.).
dc.format.page3024-3034
dc.format.volume17
dc.identifierISI:000390894700021
dc.identifier.citationCell Rep. 2016; 17(11):3024-3034
dc.identifier.doi10.1016/j.celrep.2016.11.049
dc.identifier.issn2211-1247
dc.identifier.journalCell Reports
dc.identifier.pubmedID27974214
dc.identifier.urihttp://hdl.handle.net/20.500.12105/5169
dc.language.isoeng
dc.publisherCell Press
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/618697es_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.celrep.2016.11.049
dc.repisalud.institucionCNIC
dc.repisalud.orgCNICCNIC::Grupos de investigación::Genética Funcional del Sistema de Fosforilación Oxidativa
dc.repisalud.orgCNICCNIC::Grupos de investigación::Proteómica cardiovascular
dc.repisalud.orgCNICCNIC::Unidades técnicas::Proteómica / Metabolómica
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectCYTOCHROME-C RELEASE
dc.subjectCONTACT SITE
dc.subjectORGANIZING SYSTEM
dc.subjectMITOFILIN COMPLEXES
dc.subjectAPOPTOSIS
dc.subjectMEMBRANE
dc.subjectOPA1
dc.subjectORGANIZATION
dc.subjectPATHWAY
dc.subjectFUSION
dc.titleOptic Atrophy 1 Is Epistatic to the Core MICOS Component MIC60 in Mitochondrial Cristae Shape Control
dc.typejournal article
dc.type.hasVersionVoR
dspace.entity.typePublication
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relation.isAuthorOfPublication.latestForDiscovery38fcf75a-f030-4879-ae7a-a697cff3c329

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