Meeting Abstract
Ocean acidification (OA) caused by elevated carbon dioxide is an imminent environmental stress to marine organisms, and is hypothesized to have a suite a detrimental effects. In fish, elevated carbon dioxide causes a respiratory acidosis that is compensated through ion transport pathways at the gills. This disturbance is thought to be the underlying cause of many of the effects of OA, including reduced survival in many marine fish larvae. Importantly, little is known about the development and function of acid-base pathways in marine fish larvae. We therefore sought to explore the development of acid-base pathways in a model marine fish, the red drum (Sciaenops ocellatus), and assess the role of phenotypic plasticity in early life resilience to carbon dioxide stress. We first explored the dose response effects of carbon dioxide, which resulted in significant reductions in larval survival at OA relevant partial pressures. However, a significant proportion of tested individuals also exhibited surprising resilience to carbon dioxide with approximately 50% survival when exposed to partial pressures over 10x those relevant to OA. Gene expression and confocal microscopy were used to assess acid-base pathways, which provided evidence for functional pathways and CO2-induced plasticity as early as 36 hours post-fertilization. A scanning ion electrode technique was used to verify the function of these pathways, which was evident from a dose-dependent increase of proton flux across the larval epithelium. Interestingly, proton flux was both bafilomycin-sensitive and EIPA-sensitive suggesting the presence of multiple acid excretion mechanisms, which likely contributes to the observed resilience of red drum to carbon dioxide stress.
