Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin

Jeehye Park, Sung Bae Lee, Sungkyu Lee, Yongsung Kim, Saera Song, Sunhong Kim, Eunkyung Bae, Jaeseob Kim, Minho Shong, Jin-Man Kim and Jongkyeong Chung ()
Additional contact information
Jeehye Park: National Creative Research Initiatives Center for Cell Growth Regulation
Sung Bae Lee: National Creative Research Initiatives Center for Cell Growth Regulation
Sungkyu Lee: National Creative Research Initiatives Center for Cell Growth Regulation
Yongsung Kim: National Creative Research Initiatives Center for Cell Growth Regulation
Saera Song: National Creative Research Initiatives Center for Cell Growth Regulation
Sunhong Kim: National Creative Research Initiatives Center for Cell Growth Regulation
Eunkyung Bae: GenExel, Inc.
Jaeseob Kim: Korea Advanced Institute of Science and Technology
Minho Shong: Department of Internal Medicine
Jin-Man Kim: Chungnam National University School of Medicine
Jongkyeong Chung: National Creative Research Initiatives Center for Cell Growth Regulation

Nature, 2006, vol. 441, issue 7097, 1157-1161

Abstract: Parkin penalty The PINK1 gene was recently implicated in autosomal recessive juvenile Parkinson's disease. Two groups have studied the equivalent gene in the fruitfly Drosophila, and find that it localizes to mitochondria in vivo and is essential to mitochondrial function. It also interacts genetically with parkin, another familial Parkinson's disease-related gene that encodes Parkin, an E3 ubiquitin ligase. The pink1-parkin pathway in Drosophila should provide a powerful tool for the study of the molecular mechanisms of neurodegeneration and for screening agents of possible therapeutic interest.

Date: 2006
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DOI: 10.1038/nature04788

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