Protein synthesis is defended in the mitochondrial fraction of gill but not heart in cunner (Tautogolabrus adspersus) exposed to acute hypoxia and hypothermia
The cunner, Tautogolabrus adspersus, is a north-temperate teleost which relies upon metabolic depression to survive the extreme low water temperatures of its habitat during the winter. Previous study has demonstrated a decrease in protein synthesis accompanies the metabolic depression observed at the whole animal level during seasonal low temperature exposure. As such, the objective of the current study was to determine: (i) if the response of decreased protein synthesis is conserved across environmental stressors and (ii) if the response of metabolic depression is conserved across levels of cellular organization. This was accomplished through the measurement of in vivo protein synthesis rates in the whole tissue, cytosolic and mitochondrial protein pools (reflective of nuclear encoded proteins imported into mitochondria) of heart and gill in cunner exposed to either acute low temperature (8–4°C) or acute hypoxia (10% O2 saturation). In both heart and gill, rates of protein synthesis in the whole tissue and cytosolic protein pools were substantially depressed by 80% in response to acute hypothermia. In hypoxic heart, protein synthesis was significantly decreased by 50–60% in the whole tissue, cytosolic and mitochondrial pools; however, in gill there was no significant difference in rates of protein synthesis in any cellular fraction between normoxic and hypoxic groups. Most strikingly the rate of new protein accumulation in the mitochondrial fraction of gill did not change in response to either a decrease in temperature or hypoxia. The defense of protein synthesis in the gill is most likely associated with the importance of maintaining ionic regulation and the oxidative capacity in this front line organ for gas and ion exchange.