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Optic atrophy 1 (OPA1) is a dynamin-like GTPase located in the inner mitochondrial membrane and mutations in  OPA1  are associated with autosomal dominant optic atrophy (DOA). OPA1 plays important roles in mitochondrial fusion, cristae remodeling and apoptosis. Our previous study showed that  dOpa 1 mutation caused elevated reactive oxygen species (ROS) production and resulted in damage and death of the cone and pigment cells in  Drosophila  eyes. Since ROS-induced oxidative damage to the cells is one of the primary causes of aging, in this study, we examined the effects of heterozygous  dOpa 1 mutation on the lifespan. We found that heterozygous  dOpa 1 mutation caused shortened lifespan, increased susceptibility to oxidative stress and elevated production of ROS in the whole  Drosophila . Antioxidant treatment partially restored lifespan in the male  dOpa1  mutants, but had no effects in the females. Heterozygous  dOpa 1 mutation caused an impairment of respiratory chain complex activities, especially complexes II and III, and reversible decreased aconitase activity. Heterozygous  dOpa 1 mutation is also associated with irregular and dysmorphic mitochondria in the muscle. Our results, for the first time, demonstrate the important role of OPA1 in aging and lifespan, which is most likely mediated through augmented ROS production.

Heterozygous Mutation of Opa1 in Drosophila Shortens Lifespan Mediated through Increased Reactive Oxygen Species Production