Journal
FEBS LETTERS
Volume 590, Issue 19, Pages 3309-3322Publisher
WILEY-BLACKWELL
DOI: 10.1002/1873-3468.12384
Keywords
apoptosis; crista junction; MICOS; mitochondria; Mitofilin
Funding
- Deutsche Forschungsgemeinschaft, Cluster of Excellence Frankfurt Macromolecular Complexes, Focus project
- BMBF, GerontoMitoSys
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Remodeling of crista junctions (CJs) is observed in numerous human disorders and during apoptosis. The functional interplay of OPA1 and MIC60, two key players in this context, is unclear. We show that OPA1 modulates cristae morphology but is dispensable for CJ formation. MIC60 is strongly enriched at CJs, whereas OPA1 is distributed evenly across the inner membrane. MIC60 levels are increased in OPA1(-/-) cells which show increased cellular resistance to apoptosis induction. Endogenous OPA1 and MIC60 show a physical interaction. Overall, we suggest that the regulation of CJ remodeling during apoptosis is mediated via an interplay between OPA1 and MIC60.
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