33rd Annual Student Research Conference
Interactions between neuronal activity and ALS mutations in the fruit fly, Drosophila melanogaster
Grace E. McGennis*, Alyssa R. Soles, Sydney E. Morin, and Morgan D. Payne
Dr. Brett A. Berke, Faculty Mentor
In the neurodegenerative disease amyotrophic lateral sclerosis (ALS), neurons all possess the same mutations, yet only some neurons die. We hypothesize that dying, mutant neurons are more active and spend valuable resources. Using the fruit fly Drosophila melanogaster, we are researching two ALS-linked genes called c9ORF72 and SOD1. c9ORF72 mutations produce toxic proteins that disrupt nucleocytoplasmic transport, and the loss of SOD1 causes the buildup of oxygen radicals. We increased neuronal activity by rearing flies at high temperature and by using a K+ channel null mutant. Increased neuronal activity paired with an RNA interference knockdown of SOD1 reduced the adult lifespan and increased cell death. Flies expressing toxic c9ORF72 proteins exhibited abnormal nuclear transport and synaptic growth defects, and we are checking for interactions with activity. These results indicate that excessive neuronal activity may synergize with ALS mutations to promote neurodegeneration.
Keywords: Drosophila, ALS, neurodegeneration, synapses
Topic(s):Biology
Presentation Type: Poster
Session: TBA
Location: TBA
Time: TBA