期刊
NEURODEGENERATIVE DISEASES
卷 5, 期 3-4, 页码 182-185出版社
KARGER
DOI: 10.1159/000113697
关键词
mitochondria; rotenone toxicity; Coenorhabditis elegans; familial Parkinson's disease
资金
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES015567] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS060872] Funding Source: NIH RePORTER
- NIEHS NIH HHS [ES015567, R01 ES015567] Funding Source: Medline
- NINDS NIH HHS [R01 NS060872] Funding Source: Medline
Background: Mutations in LRRK2 are among the most frequent genetic changes identified in Parkinson's disease (PD), but how LRRK2 contributes to the pathophysiology of PD is not known. Objectives: To investigate how expressing wildtype or G2019S LRRK2 modifies cellular responses to rotenone, a mitochondrial toxin. Methods: We investigated the vulnerability to mitochondrial toxins in Caenorhabditis elegans expressing wild-type or G2019S LRRK2. Results: We observed a powerful role for LRRK2 in mitochondrial biology. Overexpressing LRRK2 strongly protects C. elegans against rotenone toxicity. The G2019S LRRK2 construct also protected LRRK2 against rotenone, but to a lesser degree than wildtype LRRK2. Knockdown of Irk-1 potentiated rotenone toxicity. Conclusions: These data suggest that LRRK1/2 regulate mitochondrial physiology. Copyright (c) 2008 S. Karger AG, Basel.
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