Optic Atrophy 1 Is Epistatic to the Core MICOS Component MIC60 in Mitochondrial Cristae Shape Control
Author(s) -
Christina Glytsou,
Enrique Calvo,
Sara Cogliati,
Arpit Mehrotra,
Irene Anastasia,
Giovanni Rigoni,
Andrea Raimondi,
Norihito Shintani,
Marta Loureiro,
Jesús Vázquez,
Luca Pellegrini,
José Antonio Enrı́quez,
Luca Scorrano,
María Eugenia Soriano
Publication year - 2016
Publication title -
cell reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.264
H-Index - 154
eISSN - 2639-1856
pISSN - 2211-1247
DOI - 10.1016/j.celrep.2016.11.049
Subject(s) - epistasis , mitochondrion , biogenesis , biology , microbiology and biotechnology , mitochondrial dna , mitochondrial biogenesis , core (optical fiber) , genetics , gene , materials science , composite material
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.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom