News & Updates
Search Research Content
Resource Finder at Kennedy Krieger Institute
A free resource that provides access to information and support for individuals and families living with developmental disabilities.
Signaling Pathways Involved in 1-Octen-3-ol-Mediated Neurotoxicity in Drosophila melanogaster: Implication in Parkinson's Disease.
|Title||Signaling Pathways Involved in 1-Octen-3-ol-Mediated Neurotoxicity in Drosophila melanogaster: Implication in Parkinson's Disease.|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Inamdar AA, Masurekar P, Hossain M, Richardson JR, Bennett JW|
|Date Published||2013 Aug 20|
Previously, we have pioneered Drosophila melanogaster as a reductionist model to show that 1-octen-3-ol, a musty-smelling volatile compound emitted by fungi and other organisms, causes loss of dopaminergic neurons and Parkinson's disease-like symptoms in flies. Using our in vivo Drosophila system, the modulatory roles of important signaling pathways-JNK, Akt and the caspase-3-dependent apoptotic pathway were investigated in the context of 1-octen-3-ol-induced dopamine neurotoxicity. When heterozygous flies carrying mutant alleles for these proteins were exposed to 0.5 ppm of 1-octen-3-ol, they had shorter survival times than wild-type Drosophila. The overexpressed levels of wild-type JNK and Akt, (UAS-bsk and UAS-Akt) with TH-GAL4 and elav-GAL4 drivers improved the survival duration of exposed flies compared with controls. Thus, we found that Akt and JNK both protect against loss of dopamine activity associated with 1-octen-3-ol exposure, indicating the pro-survival role of these signaling pathways. Further, 1-octen-3-ol exposure was associated with activation of caspase 3, a hallmark for apoptosis.
|Alternate Journal||Neurotox Res|