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
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.
SUPPLEMENTAL MATERIAL
Coming soon ....
REFERENCES (32)
CITATIONS (1016)
EXTERNAL LINKS
PlumX Metrics
RECOMMENDATIONS
FAIR ASSESSMENT
Coming soon ....
JUPYTER LAB
Coming soon ....