Journal
EMBO REPORTS
Volume 11, Issue 6, Pages 459-465Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/embor.2010.50
Keywords
ADOA; apoptosis; Bnip3; mitochondrial dynamics; Opa1
Categories
Funding
- Centre National de la Recherche Scientifique
- Universite Paul Sabatier
- Retina France
- Association Francaise contre les Myopathies
- Association pour la Recherche sur le Cancer
- Ligue Contre le Cancer Haute-Garonne
- Association contre les Maladies Mitochondriales
- Ligue Nationale contre le Cancer
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Opa1 modulates mitochondrial fusion, cristae structure and apoptosis. The relationships between these functions and autosomal dominant optic atrophy, caused by mutations in Opa1, are poorly defined. We show that Bnip3 interacts with Opa1, leading to mitochondrial fragmentation and apoptosis. Fission is due to inhibition of Opa1-mediated fusion and is counteracted by Opa1 in an Mfn1-dependent manner. Bnip3-Opa1 interaction is necessary to trigger Opa1 complex disruption in a Baxand/or Bak-dependent manner, ultimately leading to apoptosis. Our results uncover a direct link between Opa1 on the inner mitochondrial membrane and the apoptotic machinery on the outer membrane that modulates fusion and cristae structure by separate mechanisms. These findings might help to unravel optic atrophy aetiology as retinal ganglion cells are particularly prone to hypoxia, an inductor of Bnip3 expression.
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