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daf-2 signaling modifies mutant sod1 toxicity in c. elegansdaf - 2信号修改sod1基因突变在秀丽隐杆线虫毒性
Daf-2 Signaling Modifies Mutant SOD1 Toxicity in C. elegans 1,2 3 1,2,4 Marco Boccitto *, Todd Lamitina , Robert G. Kalb 1 Department of Pediatrics, Division of Neurology, Children’s Hospital of Philadelphia Research Institute, Philadelphia, Pennsylvania, United States of America, 2 Department of Neuroscience, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, United States of America, 3 Department of Physiology, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America, 4 Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, United States of America Abstract The DAF-2 Insulin/IGF-1 signaling (IIS) pathway is a strong modifier of Caenorhabditis elegans longevity and healthspan. As aging is the greatest risk factor for developing neurodegenerative diseases such as Amyotrophic Lateral Sclerosis (ALS), we were interested in determining if DAF-2 signaling modifies disease pathology in mutant superoxide dismutase 1 (SOD1) expressing C. elegans. Worms with pan-neuronal G85R SOD1 expression demonstrate significantly impaired locomotion as compared to WT SOD1 expressing controls and they develop insoluble SOD1 aggregates. Reductions in DAF-2 signaling, either through a hypomorphic allele or neuronally targeted RNAi, decreases the abundance of aggregated SOD1 and results in improved locomotion in a DAF-16 dependant manner. These results suggest that manipulation of the DAF-2 Insulin/IGF-1 signaling pathway may have therapeutic potential for the treatment of ALS. Citation: Boccitto M, Lamitina T, Kalb RG (2012) Daf-2 Signaling Modifies Mutant SOD1 Toxicity in C. elegans. PLoS ONE 7(3): e33494. doi:10.1371/ journal.pone.0033494 Editor: Mikhail V. Blagosklonny, Roswell Park Cancer Insti
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