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  • Open Daily: 10am - 10pm
    Alley-side Pickup: 10am - 7pm

    3038 Hennepin Ave Minneapolis, MN
    612-822-4611

Open Daily: 10am - 10pm | Alley-side Pickup: 10am - 7pm
3038 Hennepin Ave Minneapolis, MN
612-822-4611
A Drosophila Melanogaster Model of Pink1-Associated Parkinson's Disease.

A Drosophila Melanogaster Model of Pink1-Associated Parkinson's Disease.

Yang, Yufeng

Paperback

Biology

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ISBN10: 1243609265
ISBN13: 9781243609267
Publisher: Proquest Umi Dissertation Pub
Pages: 146
Weight: 0.60
Height: 0.31 Width: 7.44 Depth: 9.69
Language: English
Mutations of gene Pink1 lead to early-onset autosomal recessive Parkinson's disease. The mechanism by which dysfunction of Pink1 leads to neurodegeneration is not understood. To understand the physiological function of Pink1 and how its dysfunction may cause Parkinson's disease, I used Drosophila melanogaster as a genetic model system to dissect out the signaling pathway Pink1 might be involved in. First I used in vivo RNA interference (RNAi) to knockdown the expression level of Drosophila Pink1 (dPink1 ). I then characterized the phenotypes caused by down-regulation of dPink1. Pathologic phenotypes include energy depletion, shortened lifespan, degeneration of selective indirect flight muscles and dopaminergic system, aberrant mitochondrial morphology. I found that the pathologic phenotypes caused by loss of function of Pink I could be rescued by overexpression of Parkin, another Parkinson's disease associated gene. In order to understand how aberrant mitochondrial morphology arises due to loss of function of Pink1, I investigated whether Pink1 might interact with mitochondrial morphogenesis/dynamics pathway. Genetic manipulations that promote mitochondrial fission suppress Drosophila Pink1 mutant phenotypes in indirect flight muscle and dopamine neurons, whereas decreased fission has opposite effects. In Drosophila and mammalian cells, overexpression of Pink1 promotes mitochondrial fission, whereas inhibition of Pink1 leads to excessive fusion. In summary, my research indicate that two Parkinson's disease genes, Pink1 and Parkin converge in a common pathway and both are required for maintaining proper mitochondria morphology and the integrity of subsets of muscle cells and dopaminergic neurons. What's more, my results have provided novel insight of the pathogenesis of Parkinson's disease and established mitochondrial fission/fusion as a paradigm for Parkinson's disease research.

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