p32 regulates mitochondrial morphology and dynamics through parkin.
Mutations in parkin were first identified in a group of Japanese patients who developed autosomal recessive juvenile Parkinsonism with clinical symptoms similar to idiopathic Parkinson's disease (PD). Parkin is an E3 ligase that targets a number of substrates for ubiquitination. Recent studies show that parkin together with PINK1, another familial-linked PD gene product, is involved in the regulation of mitochondrial dynamics in the cell. In this study, we have identified a mitochondrial protein p32 as a novel interactor of parkin in the brain. We found that p32 can regulate mitochondrial morphology and dynamics by promoting parkin degradation through autophagy. These results suggest that parkin might be an important effector in the regulation of morphology and dynamics of mitochondria.
Division of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.
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Li
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Wan
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Xie
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Chung
D000818:Animals; D001343:Autophagy / Q000502:physiology; D015153:Blotting, Western; D002352:Carrier Proteins; D002478:Cells, Cultured; D006801:Humans; D007150:Immunohistochemistry; D047468:Immunoprecipitation; D051379:Mice; D018613:Microscopy, Confocal; D008928:Mitochondria / Q000378:metabolism / Q000648:ultrastructure*; D024101:Mitochondrial Proteins / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism / Q000648:ultrastructure; D014162:Transfection; D044767:Ubiquitin-Protein Ligases / Q000378:metabolism*; D054875:Ubiquitination
C087299:C1QBP protein, human; D002352:Carrier Proteins; D024101:Mitochondrial Proteins; D044767:Ubiquitin-Protein Ligases; C111567:parkin protein