User:Heather N. Currey/Notebook/Taylor C. elegans Lab Notebook

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Project Description/Abstract

  • The effects of Disrupted Insulin Signaling on the accumulation of Age related Neuronal Aberrations in Huntington’s Disease Model
  • The proposed research aims to establish the effects of the insulin-like signaling pathway as part of a larger project to elucidate the relationship between neurodegeneration and aging and insulin signaling. This work will be done on a genetically engineered strain of the nematode Caenorhabditis elegans modeling Huntington’s disease. Huntington’s disease in humans is a heritable neurodegenerative disorder caused by a mutation in the huntingtin protein resulting in 38 or more polygutamine (polyQ) repeats leading to protein aggregation within neurons, impaired motor function, cognitive decline and premature aging. Others have shown that parts of the nervous system in C. elegans deteriorate with age and that this deterioration is mediated, at least in part, by the insulin-like signaling pathway in the worms (Toth, 2012), (Tank, 2011). My lab is currently working on a screen of 39 genes involved in the insulin-like pathway to distinguish genes that profoundly affect the neuronal aberrations compared to control. I will test the hypothesis that specific signaling proteins within the insulin-like pathway are involved in huntingtin protein aggregation and determine their association with aging. To test this hypothesis I will use RNA interference (RNAi) knockdown technique, which uses double stranded RNA inserted into the cell to prevent gene transcription.

Notes

  • Seeded plates with RNAi ins4,7,8,9 (6 plates each)
  • Imaged Ins-3 between 4:30 and 7:30
  • n imaged =
  • Egglay start: 10:40 end: n=20



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