Molecular Biology Commons^™

Reactive Oxygen Species-Mediated Neurodegeneration Is Independent Of The Ryanodine Receptor In Caenorhabditis Elegans, Lyndsay E.A. Young, Daniel C. Williams

Journal of the South Carolina Academy of Science

Despite the significant impacts on human health caused by neurodegeneration, our understanding of the degeneration process is incomplete. The nematode Caenorhabditis elegans is 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 gene unc-68, which encodes the ryanodine receptor, abolishes excitotoxic cell death, indicating a role for calcium (Ca²⁺) signaling in neurodegeneration. We tested the requirement for unc-68 in ROS-mediated neurodegeneration using the …

Regulation Of The Ampa Glutamate Receptor Homolog Glr-1 At The Endoplasmic Reticulum In C. Elegans., Sam Witus, Lina Dahlberg

Scholars Week

In C. elegans, the glutamate receptor GLR-1 functions in the nervous system to decode environmental stimuli and sensory experiences, and to regulate locomotion and the formation of long-term memory. C. elegans GLR-1 is homologous to mammalian glutamate receptors, and we can use this simple organism as a system to better understand the life cycle of human receptors (1). Because GLR-1 is a membrane protein, it is first assembled in the interior of a neuron, and then it is transported to the membrane at the surface of the cell so that it can receive chemical signals (glutamate) from the environment. Currently, …

The Effects Of Supplemented Metabolites On Lifespan And Stress Response Pathways In Caenorhabditis Elegans, Clare B. Edwards

USF Tampa Graduate Theses and Dissertations

Understanding how metabolites contribute to anaplerosis, antioxidant effects, and hormetic pathways during aging is fundamental to creating supplements and dietary habits that may decrease age-associated disease and decline, thus improving the quality of life in old age. In order to uncover metabolic pathways that delay aging, the effects of large sets of metabolites associated with mitochondrial function on lifespan were investigated.

Malate, the tricarboxylic acid (TCA) cycle metabolite, increased lifespan and thermotolerance in C. elegans. Addition of fumarate and succinate also extended lifespan and all three metabolites activated nuclear translocation of the cytoprotective DAF-16/FOXO transcription factor and protected from paraquat-induced …