Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 378, Issue 3, Pages 518-523Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2008.11.086
Keywords
PINK1; parkin; Parkinson's disease; Mitochondria
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Funding
- Korean Ministry of Education, Science and Technology/KOSEF [R16-2001-002-01001-0]
- National Research Foundation of Korea [2001-0046413, R16-2001-002-01001-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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The two Parkinson's disease (PD) genes, PTEN-induced kinase 1 (PINK1) and parkin, are linked in a common pathway which affects mitochondrial integrity and function. However, it is still not known what this pathway does in the mitochondria. Therefore, we investigated its physiological function in Drosophila. Because Drosophila PINK1 and parkin Mutants show changes in mitochondrial morphology in both indirect flight muscles and dopaminergic neurons, we here investigated whether the PINK1-Parkin pathway genetically interacts with the regulators of mitochondrial fusion and fission such as Drp1, which promotes mitochondrial fission, and Opal or Marf, which induces mitochondrial fusion. Surprisingly, Drosophila PINK1 and parkin mutant phenotypes were markedly suppressed by overexpression of Drp1 OF downregulation of Opal or Marf, indicating that the PINK1-Parkin pathway regulates mitochondrial remodeling process in the direction of promoting mitochondrial fission. Therefore, we strongly suggest that mitochondrial fusion and fission process could be a prominent therapeutic target for the treatment of PD. (C) 2008 Elsevier Inc. All rights reserved.
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