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Título
Optic Atrophy 1 Is Epistatic to the Core MICOS Component MIC60 in Mitochondrial Cristae Shape Control
Autor(es)
Glytsou, Christina | Calvo, Enrique CNIC | Cogliati, Sara CNIC | Mehrotra, Arpit | Anastasia, Irene | Rigoni, Giovanni | Raimondi, Andrea | Shintani, Norihito | Loureiro, Marta CNIC | Vazquez, Jesus CNIC | Pellegrini, Luca | Enriquez, Jose Antonio CNIC | Scorrano, Luca | Soriano, Maria Eugenia
Fecha de publicación
2016
Cita
Cell Rep. 2016; 17(11):3024-3034
Idioma
Inglés
Tipo de documento
journal article
Resumen
The 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.
Palabras clave
CYTOCHROME-C RELEASE | CONTACT SITE | ORGANIZING SYSTEM | MITOFILIN COMPLEXES | APOPTOSIS | MEMBRANE | OPA1 | ORGANIZATION | PATHWAY | FUSION
Versión en línea
DOI
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