ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Loss-of-function analysis suggests that Omi/HtrA2 is not an essential component of the PINK1/PARKIN pathway in vivo.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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41 citing papers in PubMed, 85 citations in OpenAlex.
- A central role for PINK1 in governing local mitochondrial biogenesis and degradation in neurons.Cellular and molecular life sciences : CMLS · 2026Review
- Oral intake of aripiprazole compromises male fertility in Drosophila.Biology direct · 2025Article
- Mitochondrial Differentiation during Spermatogenesis: Lessons fromInternational journal of molecular sciences · 2024Review
- Proteolysis in Reproduction: Lessons From Gene-Modified Organism Studies.Frontiers in endocrinology · 2022Review
- Generation, Analyzing andBio-protocol · 2020Article
- Enhancing glycolysis attenuates Parkinson's disease progression in models and clinical databases.The Journal of clinical investigation · 2019Article
- Atg1-mediated autophagy suppresses tissue degeneration inMolecular biology of the cell · 2018Article
- Article
- Bar-coding neurodegeneration: identifying subcellular effects of human neurodegenerative disease proteins usingDisease models & mechanisms · 2017Article
- Review
- Article
- Oxidative stress-induced signaling pathways implicated in the pathogenesis of Parkinson's disease.Neuromolecular medicine · 2014Review
- BAG5 protects against mitochondrial oxidative damage through regulating PINK1 degradation.PloS one · 2014Article
- X11/Mint genes control polarized localization of axonal membrane proteins in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Function and characteristics of PINK1 in mitochondria.Oxidative medicine and cellular longevity · 2013Review
- Drosophila as a model to study mitochondrial dysfunction in Parkinson's disease.Cold Spring Harbor perspectives in medicine · 2012Review
- PINK1 as a molecular checkpoint in the maintenance of mitochondrial function and integrity.Molecules and cells · 2012Review
- Mitochondrial dynamics and Parkinson's disease: focus on parkin.Antioxidants & redox signaling · 2012Review
- Mitochondrial quality control: a matter of life and death for neurons.The EMBO journal · 2012Review
- Mitochondrial dysfunction precedes other sub-cellular abnormalities in an in vitro model linked with cell death in Parkinson's disease.Neurotoxicity research · 2012Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Recently, a mutation in the mitochondrial protease Omi/HtrA2, G399S, was found in sporadic Parkinson's disease (PD) patients, leading to the designation of Omi/HtrA2 as PD locus 13 (PARK13). G399S reportedly results in reduced Omi protease activity. In vitro studies have suggested that Omi/HtrA2 acts downstream of PINK1, mutations in which mediate recessive forms of PD. We, as well as other, have previously shown that the Drosophila homologs of the familial PD genes, PINK1 (PARK6) and PARKIN (PARK2), function in a common genetic pathway to regulate mitochondrial integrity and dynamics. Whether Omi/HtrA2 regulates mitochondrial integrity and whether it acts downstream of PINK1 in vivo remain to be explored. Here, we show that Omi/HtrA2 null mutants in Drosophila, in contrast to pink1 or parkin null mutants, do not show mitochondrial morphological defects. Extensive genetic interaction studies do not provide support for models in which Omi/HtrA2 functions in the same genetic pathway as pink1, or carries out partially redundant functions with pink1, at least with respect to regulation of mitochondrial integrity and dynamics. Furthermore, Omi/HtrA2 G399S retains significant, if not full, function of Omi/HtrA2, compared with expression of protease-compromised versions of the protein. In light of recent findings showing that G399S can be found at comparable frequencies in PD patients and healthy controls, we do not favor a hypothesis in which Omi/HtrA2 plays an essential role in PD pathogenesis, at least with respect to regulation of mitochondrial integrity in the pink1/parkin pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.