ArticlePloS one2009
Heterozygous mutation of Drosophila Opa1 causes the development of multiple organ abnormalities in an age-dependent and organ-specific manner.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 45 citations in OpenAlex.
- OPA1 Deficiency Impairs NGF Signaling and Drives Sympathetic Neurodegeneration.JACC. Basic to translational science · 2026Article
- A High-Fat Diet Induces Oxidative Stress in OPA1Antioxidants (Basel, Switzerland) · 2025Article
- Article
- OPA1 deficiency impairs oxidative metabolism in cycling cells, underlining a translational approach for degenerative diseases.Disease models & mechanisms · 2023Article
- Mitochondrial Neurodegeneration: Lessons fromBiomolecules · 2023Review
- Short-form OPA1 is a molecular chaperone in mitochondrial intermembrane space.Science China. Life sciences · 2022Article
- Mitochondrial Dysfunction: An Emerging Link in the Pathophysiology of Cardiorenal Syndrome.Frontiers in cardiovascular medicine · 2022Review
- OMA1-An integral membrane protease?Biochimica et biophysica acta. Proteins and proteomics · 2021Review
- Dominant Optic Atrophy (DOA): Modeling the Kaleidoscopic Roles of OPA1 in Mitochondrial Homeostasis.Frontiers in neurology · 2021Review
- The Role of Mitochondria in Optic Atrophy With Autosomal Inheritance.Frontiers in neuroscience · 2021Review
- Loss of functional OPA1 unbalances redox state: implications in dominant optic atrophy pathogenesis.Annals of clinical and translational neurology · 2016Article
- Cardiac deficiency of single cytochrome oxidase assembly factor scox induces p53-dependent apoptosis in a Drosophila cardiomyopathy model.Human molecular genetics · 2015Article
- Disturbed mitochondrial dynamics and neurodegenerative disorders.Nature reviews. Neurology · 2015Review
- Altered skeletal muscle mitochondrial biogenesis but improved endurance capacity in trained OPA1-deficient mice.The Journal of physiology · 2013Article
- 3D chromatin interactions organize Yan chromatin occupancy and repression at the even-skipped locus.Genes & development · 2013Article
- Mitochondrial dynamics in the adult cardiomyocytes: which roles for a highly specialized cell?Frontiers in physiology · 2013Article
- Down-regulation of OPA1 alters mouse mitochondrial morphology, PTP function, and cardiac adaptation to pressure overload.Cardiovascular research · 2012Article
- Mitochondrial optic neuropathies - disease mechanisms and therapeutic strategies.Progress in retinal and eye research · 2011Review
- Mitochondrial disorders and the eye.Eye and brain · 2011Review
- Mitochondrial oxidative phosphorylation compensation may preserve vision in patients with OPA1-linked autosomal dominant optic atrophy.PloS one · 2011Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Optic Atrophy 1 (OPA1) is a ubiquitously expressed dynamin-like GTPase in the inner mitochondrial membrane. It plays important roles in mitochondrial fusion, apoptosis, reactive oxygen species (ROS) and ATP production. Mutations of OPA1 result in autosomal dominant optic atrophy (DOA). The molecular mechanisms by which link OPA1 mutations and DOA are not fully understood. Recently, we created a Drosophila model to study the pathogenesis of optic atrophy. Heterozygous mutation of Drosophila OPA1 (dOpa1) by P-element insertion results in no obvious morphological abnormalities, whereas homozygous mutation is embryonic lethal. In eye-specific somatic clones, homozygous mutation of dOpa1 causes rough (mispatterning) and glossy (decreased lens deposition) eye phenotypes in adult Drosophila. In humans, heterozygous mutations in OPA1 have been associated with mitochondrial dysfunction, which is predicted to affect multiple organs. In this study, we demonstrated that heterozygous dOpa1 mutation perturbs the visual function and an ERG profile of the Drosophila compound eye. We independently showed that antioxidants delayed the onset of mutant phenotypes in ERG and improved larval vision function in phototaxis assay. Furthermore, heterozygous dOpa1 mutation also caused decreased heart rate, increased heart arrhythmia, and poor tolerance to stress induced by electrical pacing. However, antioxidants had no effects on the dysfunctional heart of heterozygous dOpa1 mutants. Under stress, heterozygous dOpa1 mutations caused reduced escape response, suggesting abnormal function of the skeletal muscles. Our results suggest that heterozygous mutation of dOpa1 shows organ-specific pathogenesis and is associated with multiple organ abnormalities in an age-dependent and organ-specific manner.
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Registered trials
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