2026-06-14T13:00:31Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/51692024-09-27T09:30:33Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605col_20.500.12105_19607

00925njm 22002777a 4500 dc Glytsou, Christina author Calvo, Enrique author Cogliati, Sara author Mehrotra, Arpit author Anastasia, Irene author Rigoni, Giovanni author Raimondi, Andrea author Shintani, Norihito author Loureiro, Marta author Vazquez, Jesus author Pellegrini, Luca author Enriquez, Jose Antonio author Scorrano, Luca author Soriano, Maria Eugenia author 2016 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. Cell Rep. 2016; 17(11):3024-3034 10.1016/j.celrep.2016.11.049 2211-1247 Cell Reports 27974214 http://hdl.handle.net/20.500.12105/5169 CYTOCHROME-C RELEASE CONTACT SITE ORGANIZING SYSTEM MITOFILIN COMPLEXES APOPTOSIS MEMBRANE OPA1 ORGANIZATION PATHWAY FUSION Optic Atrophy 1 Is Epistatic to the Core MICOS Component MIC60 in Mitochondrial Cristae Shape Control