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Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin

Author

Listed:
  • Ira E. Clark

    (Brain Research Institute, The David Geffen School of Medicine, University of California)

  • Mark W. Dodson

    (Brain Research Institute, The David Geffen School of Medicine, University of California)

  • Changan Jiang

    (Brain Research Institute, The David Geffen School of Medicine, University of California)

  • Joseph H. Cao

    (Brain Research Institute, The David Geffen School of Medicine, University of California)

  • Jun R. Huh

    (California Institute of Technology)

  • Jae Hong Seol

    (Seoul National University)

  • Soon Ji Yoo

    (Kyung Hee Institute of Age-related and Brains Disease, Kyung Hee University)

  • Bruce A. Hay

    (California Institute of Technology)

  • Ming Guo

    (Brain Research Institute, The David Geffen School of Medicine, University of California)

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.

Suggested Citation

  • Ira E. Clark & Mark W. Dodson & Changan Jiang & Joseph H. Cao & Jun R. Huh & Jae Hong Seol & Soon Ji Yoo & Bruce A. Hay & Ming Guo, 2006. "Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin," Nature, Nature, vol. 441(7097), pages 1162-1166, June.
    • Handle: RePEc:nat:nature:v:441:y:2006:i:7097:d:10.1038_nature04779
    DOI: 10.1038/nature04779
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    Cited by:

    1. Vanitha Nithianandam & Hassan Bukhari & Matthew J. Leventhal & Rachel A. Battaglia & Xianjun Dong & Ernest Fraenkel & Mel B. Feany, 2023. "Integrative analysis reveals a conserved role for the amyloid precursor protein in proteostasis during aging," Nature Communications, Nature, vol. 14(1), pages 1-19, December.
    2. Marc Thilo Figge & Andreas S Reichert & Michael Meyer-Hermann & Heinz D Osiewacz, 2012. "Deceleration of Fusion–Fission Cycles Improves Mitochondrial Quality Control during Aging," PLOS Computational Biology, Public Library of Science, vol. 8(6), pages 1-18, June.
    3. Huan Yang & Caroline Sibilla & Raymond Liu & Jina Yun & Bruce A. Hay & Craig Blackstone & David C. Chan & Robert J. Harvey & Ming Guo, 2022. "Clueless/CLUH regulates mitochondrial fission by promoting recruitment of Drp1 to mitochondria," Nature Communications, Nature, vol. 13(1), pages 1-19, December.
    4. Jenny Zhe Liao & Hyung-lok Chung & Claire Shih & Kenneth Kin Lam Wong & Debdeep Dutta & Zelha Nil & Catherine Grace Burns & Oguz Kanca & Ye-Jin Park & Zhongyuan Zuo & Paul C. Marcogliese & Katherine S, 2024. "Cdk8/CDK19 promotes mitochondrial fission through Drp1 phosphorylation and can phenotypically suppress pink1 deficiency in Drosophila," Nature Communications, Nature, vol. 15(1), pages 1-19, December.
    5. Yunpeng Huang & Zhihui Wan & Yinglu Tang & Junxuan Xu & Bretton Laboret & Sree Nallamothu & Chenyu Yang & Boxiang Liu & Rongze Olivia Lu & Bingwei Lu & Juan Feng & Jing Cao & Susan Hayflick & Zhihao W, 2022. "Pantothenate kinase 2 interacts with PINK1 to regulate mitochondrial quality control via acetyl-CoA metabolism," Nature Communications, Nature, vol. 13(1), pages 1-16, December.
    6. Federico Miozzo & Eva P. Valencia-Alarcón & Luca Stickley & Michaëla Majcin Dorcikova & Francesco Petrelli & Damla Tas & Nicolas Loncle & Irina Nikonenko & Peter Bou Dib & Emi Nagoshi, 2022. "Maintenance of mitochondrial integrity in midbrain dopaminergic neurons governed by a conserved developmental transcription factor," Nature Communications, Nature, vol. 13(1), pages 1-18, December.

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