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Cited by 1,203Parkinson's Disease Mechanisms and TreatmentsMitochondrial Function and PathologyNuclear Receptors and Signaling

The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.

Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants

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Greene, Jessica C., Whitworth, Alexander J., Kuo, Isabella, Andrews, Laurie A., Feany, Mel B., Pallanck, Leo J.·2003·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.0737556100PMC PMC153051
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Abstract

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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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
ORCID
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
DOI
10.1073/pnas.0737556100
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
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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