Meeting Abstract
Co-adapted cellular processes that overcame metabolic toxicity resulting from use of highly reactive molecular oxygen, a challenge exacerbated by electrophilic xenobiotics and abiotic agents such as UVR, are crucial to the success of aerobic life on Earth. Oxidative stress is the product of damage to molecules such as proteins, lipids, and nucleic acids caused by reactive oxygen species (ROS). To survive this stressful environment, long-lived species utilize a variety of antioxidant compounds and have evolved many enzymes that inactivate ROS. The expression of enzymes to protect against ROS is coordinated by a small number of related nuclear transcription factors, the most important of these being the master regulator, Nrf2. Regulation of Nrf2 is thought to be largely driven by Keap1. Upon exposure to ROS, Nrf2 dissociates from Keap1 and is shuttled to the nucleus where it activates its target genes. Keap1-Nrf2 interaction is conserved in Drosophila and vertebrates but little is known about this system in early branching metazoans. Using genomic, transcriptomic and proteomic data, we analyzed Keap1/Nrf2 orthologs in several cnidarian taxa as well as other early-diverging metazoans. We also examine other associated oxidative stress response proteins in both parasitic and free-living cnidarians, which may experience different levels of metabolic and environmental toxicity due to diverse life-histories. Investigation of Nrf2 regulation of oxidative stress in basal lineages may advance human medical intervention as well as our understanding of metazoan evolution.
