Investigating convergent actions of genes linked to familial Parkinson's disease.
[No authors listed]
摘要
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 wild-type 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 wild-type LRRK2. Knockdown of lrk-1 potentiated rotenone toxicity. CONCLUSIONS:These data suggest that LRRK1/2 regulate mitochondrial physiology.
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基因功能
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原始数据
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文献解读
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