OPA1 functionally interacts with MIC60 but is dispensable for crista junction formation

被引：69
|
作者：
Barrera, Miguel [1 ]
Koob, Sebastian [1 ]
Dikov, Daniel [1 ]
Vogel, Frank [2 ]
Reichert, Andreas S. [1 ,3 ]
机构：
[1] Goethe Univ Frankfurt, Buchmann Inst Mol Life Sci, Mitochondrial Biol, Frankfurt, Germany
[2] Max Delbruck Ctr Mol Med, Berlin, Germany
[3] Univ Dusseldorf, Fac Med, Inst Biochem & Mol Biol 1, Univ Str 1, D-40225 Dusseldorf, Germany
来源：
FEBS LETTERS | 2016年 / 590卷 / 19期
关键词：
apoptosis; crista junction; MICOS; mitochondria; Mitofilin; MITOCHONDRIAL INNER-MEMBRANE; DOMINANT OPTIC ATROPHY; DYNAMIN-RELATED GTPASE; CYTOCHROME-C RELEASE; M-AAA PROTEASE; MITOFILIN COMPLEXES; CONTACT SITE; FUSION; APOPTOSIS; MORPHOLOGY;
D O I：
10.1002/1873-3468.12384
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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.
引用
收藏
页码：3309 / 3322
页数：14
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