title: Reactive oxygen species-mediated neurodegeneration is independent of the ryanodine receptor inCaernorhabditis elegans.
abstract: Despite the significant impacts on human health caused by neurodegeneration, our understanding of the degeneration process is incomplete. The nematodeCaenorhabditis elegansis emerging as a genetic model organism well suited for identification of conserved cellular mechanisms and molecular pathways of neurodegeneration. Studies in the worm have identified factors that contribute to neurodegeneration, including excitotoxicity and stress due to reactive oxygen species (ROS). Disruption of the geneunc-68, which encodes the ryanodine receptor, abolishes excitotoxic cell death, indicating a role for calcium (Ca2+) signaling in neurodegeneration. We tested the requirement forunc-68in ROS-mediated neurodegeneration using the genetically encoded photosensitizer KillerRed. Upon illumination of KillerRed expressing animals to produce ROS, we observed similar levels of degeneration in wild-type andunc-68mutant strains. Our results indicate that ROS-mediated cell death is independent ofunc-68and suggest multiple molecular pathways of neurodegeneration.
authors.affiliation: Department of Biology, Coastal Carolina University, Conway, SC 29528.
authors.forename: Lyndsay Ea
authors.initials: LE
authors.lastname: Young
authors.affiliation: Department of Biology, Coastal Carolina University, Conway, SC 29528.
authors.forename: Daniel C
authors.initials: DC
authors.lastname: Williams