Ploidy impacts the response of Chinook salmon (𝘖𝘯𝘤𝘰𝘳𝘩𝘺𝘯𝘤𝘩𝘶𝘴 𝘵𝘴𝘩𝘢𝘸𝘺𝘵𝘴𝘤𝘩𝘢) to pathogen and thermal stress

Abstract

As climate change continues to reduce wild salmon populations, global reliance on aquaculture will become increasingly essential to sustain food availability. However, the environmental implications of aquaculture in causing Pacific salmon stock declines are becoming more apparent and as such the industry needs to transition to practices that would reduce negative impacts on wild fishes. Widespread utilization of sterile triploid fishes offers an alternative to normal diploid fish since they are unable to breed with wild population and are less likely to interact with wild fishes. Triploid salmonids have an extra set of chromosomes that prevent them from producing viable gametes, while also maintaining flesh quality for longer due to lack of nutrient deposition from muscle to eggs during sexual maturation. When farmed under optimal conditions, triploid fish perform similarly to diploids; however, when conditions become suboptimal (e.g. high temperature & infection with pathogens) triploids have reduced survival. The reasons for this reduced performance are mostly unknown, so this thesis aimed to investigate the molecular impacts of increased ploidy in Chinook salmon (Oncorhynchus tshawytscha). Specifically, the response of microRNA (miRNA) and protein coding mRNAs were investigated before and after exposure to pathogenic and thermal stress. MiRNAs are small, non-coding RNAs that bind to specific mRNA molecules and reduce protein translation. I hypothesized that diploid and triploid salmonids have subtle differences in molecular (miRNA, mRNA) indices that are exacerbated by changes in the environment (pathogens and temperature), which results in their poorer performance in response to stress. Chapter 2 investigated the miRNA responses in three immune tissues (hindgut, head kidney, and spleen) before and after exposure to Vibrio anguillarum, a common pathogen Chinook experience in open-sea net pens. Overall, ploidy had minimal impacts on miRNA abundances prior to stress. Abundance of miRNAs were altered in both ploidies after Vibrio exposure to support immune function. Just prior to Vibrio-induced mortality, the spleen of triploid fishes had altered miRNA abundances which identified that in triploids, the spleen is likely associated with their reduced immune competence. Chapter 3 investigated the immune mRNA responses in gill and heart ventricle before and after recovery from acute thermal stress. Triploid gills likely have altered pathogen sensing based on reduced pattern recognition receptor mRNA abundance. Tissue specific alterations after thermal stress provided insight into immune dynamics during a cellular heat-shock response. Specifically, pro-inflammatory cytokine mRNA abundance was elevated after recovery from thermal stress. The immune genes measured are likely thermally responsive in a time-dependent manner based on their variability after recovery from thermal stress. Chapter 4 investigated the cardiorespiratory impacts of increased ploidy before and after a critical thermal maximum (CTmax) trial. In agreement with previous studies, triploid hearts became arrhythmic at lower temperatures indicating that their hearts are less resilient to acute changes in temperature. Additionally, ventricle expression of cardiorespiratory genes was altered in triploid fish, implicating that this tissue is associated with their reduced thermal performance. Overall, this thesis provides evidence for the molecular dysregulation associated with increased ploidy in Chinook salmon. These impacts are minimal under normal conditions but exacerbated by pathogenic and thermal stress. The results here provide targets for aquaculture to develop breeding programs or therapeutics that can be used to improve health and well-being of salmonids, including triploids, in response to climate change.