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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, José Antonio 
dc.contributor.authorScorrano, Luca
dc.contributor.authorSoriano, Maria Eugenia
dc.date.accessioned2017-10-20T10:33:50Z
dc.date.available2017-10-20T10:33:50Z
dc.date.issued2016
dc.identifierISI:000390894700021
dc.identifier.citationCell Rep. 2016; 17(11):3024-3034
dc.identifier.issn2211-1247
dc.identifier.urihttp://hdl.handle.net/20.500.12105/5169
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.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.language.isoeng
dc.publisherCELL PRESS
dc.relation.isversionofPublisher's version
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.typeArtículo
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID27974214
dc.format.volume17
dc.format.page3024-3034
dc.identifier.doi10.1016/j.celrep.2016.11.049
dc.contributor.funderTelethon-Italy
dc.contributor.funderEC-European Commission
dc.contributor.funderEuropean Research Council
dc.contributor.funderMinistero dell'Istruzione dell'Università e della Ricerca (Italy)
dc.contributor.funderMinistero della Salute (Italy)
dc.contributor.funderUniversity of Padua
dc.description.peerreviewed
dc.relation.publisherversionhttps://doi.org/10.1016/j.celrep.2016.11.049
dc.identifier.journalCell Reports
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.repisalud.institucionCNIC
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/618697es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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