Interactions Between Neuronal Activity and SOD1 Mutations in the Fruit Fly, Drosophila melanogaster
The superoxide dismutase gene (SOD1) encodes a protein that eliminates oxygen radicals in cells. In the fruit fly Drosophila melanogaster, SOD1 mutations increase sensitivity to oxidative stressors, which may be related to a reduced lifespan compared to controls. We are testing whether excessive action potential firing might worsen the effects of an SOD1 knockdown by RNA interference. Both high temperature rearing and Shaker (Sh) K+ channel mutations increase action potential firing. A Sh mutation and SOD1 knockdown reduced the adult lifespan, and SOD1 flies reared at high temperature also lived half as long as controls. We then found evidence of increased cell death due to the combined manipulations, as temperature-reared SOD1 knockdowns showed an abnormal increase in TUNEL staining of larval brain. These results indicate that excessive neuronal activity may produce oxygen radicals or may increase neuronal sensitivity to oxygen radicals when SOD1 is suppressed.
Keywords: Neuroscience, Fruit flies, Cell death, Superoxide dismutase, Stress
Topic(s):Biology
Presentation Type: Oral Paper
Session: 108-1
Location: MC 209
Time: 8:30