Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants
Male
0301 basic medicine
Sequence Homology, Amino Acid
Ubiquitin-Protein Ligases
Longevity
Molecular Sequence Data
Apoptosis
Parkinson Disease
Spermatids
Recombinant Proteins
Mitochondria
Ligases
03 medical and health sciences
Mutagenesis
Nerve Degeneration
Animals
Drosophila
Amino Acid Sequence
Cloning, Molecular
Muscle, Skeletal
Sequence Alignment
DOI:
10.1073/pnas.0737556100
Publication Date:
2003-04-01T19:25:08Z
AUTHORS (6)
ABSTRACT
Parkinson's disease (PD) is a common neurodegenerative disorder characterized by loss of dopaminergic neurons in the substantia nigra. Several lines evidence strongly implicate mitochondrial dysfunction as major causative factor PD, although molecular mechanisms responsible for are poorly understood. Recently, loss-of-function mutations parkin gene, which encodes ubiquitin-protein ligase, were found to underlie familial form PD known autosomal recessive juvenile parkinsonism (AR-JP). To gain insight into mechanism selective cell death AR-JP, we have created Drosophila model this disorder. null mutants exhibit reduced lifespan, locomotor defects, and male sterility. The defects derive from apoptotic muscle subsets, whereas sterile phenotype derives spermatid individualization defect at late stage spermatogenesis. Mitochondrial pathology earliest manifestation degeneration prominent characteristic individualizing spermatids mutants. These results indicate that tissue-specific phenotypes observed result raise possibility similar impairment triggers AR-JP.
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