[
International Worm Meeting,
2017]
The innate immune system is a broadly conserved defense mechanism inherent to nearly all multicellular organisms. Production of Reactive Oxidative Species, or ROS, is a facet of the immune system that can damage both pathogen and host cells in response to infection. To protect itself from the oxidative stress resulting from infection-dependent ROS, host cells must coordinate a detoxification response; however, the mechanisms for this type of innate immune response are not well understood. In C. elegans, the Nrf transcription factor SKN-1 is a master regulator of the infection-independent oxidative stress response, activating a collection of genes that can detoxify ROS and repair damage to cells. We know of several proteins that regulate SKN-1 activity, including WDR-23, which is part of a ubiquitin-ligase complex that negatively regulates SKN-1. Even though SKN-1 is also known to play a role in infection-induced oxidative stress, we do not yet have a clear understanding of how this response is regulated. One possible candidate for regulation is FSHR-1, a G-protein coupled receptor that is known to play multiple roles in pathogenic defense and induces at least one SKN-1 target detoxification gene. However, the relationship between FSHR-1, SKN-1, and WDR-23 has not yet been elucidated. Using infection survival, pathogen avoidance, and oxidative stress reporter assays, we will determine how these proteins interact in response to infection-dependent oxidative stress.