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Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants
Open accessAbstract
Parkinson's disease (PD) is a common neurodegenerative disorder characterized by loss of dopaminergic neurons in the substantia nigra. Several lines of evidence strongly implicate mitochondrial dysfunction as a major causative factor in PD, although the molecular mechanisms responsible for mitochondrial dysfunction are poorly understood. Recently, loss-of-function mutations in the parkin gene, which encodes a ubiquitin-protein ligase, were found to underlie a familial form of PD known as autosomal recessive juvenile parkinsonism (AR-JP). To gain insight into the molecular mechanism responsible for selective cell death in AR-JP, we have created a Drosophila model of this disorder. Drosophila parkin null mutants exhibit reduced lifespan, locomotor defects, and male sterility. The locomotor defects derive from apoptotic cell death of muscle subsets, whereas the male sterile phenotype derives from a spermatid individualization defect at a late stage of spermatogenesis. Mitochondrial pathology is the earliest manifestation of muscle degeneration and a prominent characteristic of individualizing spermatids in parkin mutants. These results indicate that the tissue-specific phenotypes observed in Drosophila parkin mutants result from mitochondrial dysfunction and raise the possibility that similar mitochondrial impairment triggers the selective cell loss observed in AR-JP.
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“Conversely, reduction of mitophagy caused by the ablation of PINK and Parkin induces mitochondrial dysfunction and increased sensitivity to oxidative stress followed by muscle degeneration [225–228].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [225]
In the citing paper
“Both excessive autophagy [140, 186] and the deficient degradation of cytosolic components [225, 226] contribute to muscle atrophy.”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [225]
In the citing paper
“whereas Parkin loss-of-function in Drosophila resulted in a decreased lifespan and increased locomotor defects [157,158].”
From Mitochondrial Dynamics and Mitophagy in Skeletal Muscle Health and Aging (2021) · cites this paper as [157]
In the citing paper
“Although there are conflicting data regarding the specific effects of these proteins on mitochondrial morphology in mammalian cells, extensive studies in Drosophila revealed that knocking out either gene caused muscle degeneration that was associated with enlarged mitochondria (Clark et al., 2006; Greene et al., 2003).”
From New insights into the role of mitochondria in aging: mitochondrial dynamics and more (2010) · cites this paper as Greene et al., 2003
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Metadata
- Authors
- Greene, J. C., Whitworth, A. J., Kuo, I., Andrews, L. A., Feany, M. B., & Pallanck, L. J.
- Affiliations
- Brigham and Women's Hospital (US)
- Department of Genome Sciences, University of Washington, P.O. Box 357730, Seattle, WA 98195; and Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2003-03-17
- Volume
- 100
- Issue
- 7
- Pages
- 4078-4083
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC153051
- OpenAlex
- W2055124287
- Cited by
- 1,203
- References
- 34
- Citations by year
- 2026: 17 · 2025: 29 · 2024: 34 · 2023: 38 · 2022: 49 · 2021: 64 · 2020: 68 · 2019: 50 · 2018: 64 · 2017: 54 · 2016: 69 · 2015: 56 · 2014: 55 · 2013: 64 · 2012: 67
- FWCI
- 27.97
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (R01NS041780, 1R01NS41780-01, 1R01NS41536-01, R01NS041536)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- Parkin, Parkinson's disease, autosomal recessive juvenile parkinsonism, mitochondrial dysfunction, muscle degeneration, apoptosis, Drosophila model, ubiquitin-protein ligase, spermatid individualization, male sterility, locomotion defects, lifespan, selective cell death
- MeSH terms
- Amino Acid Sequence, Animals, Cloning, Molecular, Drosophila, Ligases, Longevity, Male, Mitochondria, Molecular Sequence Data, Nerve Degeneration, Parkinson Disease, Recombinant Proteins, Spermatids, Mutagenesis, Sequence Alignment, Apoptosis, Sequence Homology, Amino Acid, Muscle, Skeletal, Ubiquitin-Protein Ligases
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