Mitochondrial mechanisms of cold adaptation in cod (Gadus morhuaL.) populations from different climatic zones

Abstract

SUMMARYAdjustments in mitochondrial properties and capacities are crucial in acclimatization to seasonal cold as well as in evolutionary cold adaptation of marine ectotherms. To examine whether gene expression mechanisms contribute to different settings of aerobic capacities in populations of cod (Gadus morhua) along a latitudinal cline, maximum activities of key enzymes of mitochondrial metabolism and their respective mRNA levels were compared in white muscle and liver of cold (4°C) and warm (10°C) acclimated individuals from cod populations of the North Sea and the Barents Sea,respectively. In white muscle, cold acclimation caused a parallel increase in citrate synthase (CS) and in cytochrome c oxidase (COX) activities,but with a much larger effect in the cold eurythermal Arctic population. In liver, cold acclimation was accompanied by increments in CS activities, but differences between populations were minor. Overall COX activities in liver were not affected by cold acclimation, but were higher in the cold adapted population. In both populations increments in muscle CS capacities were tightly correlated with elevated mRNA levels, suggesting transcriptional control of citrate synthase levels in muscle. In liver, CS mRNA levels differed between populations but were not affected by cold acclimation, so that post-transcriptional control may contribute to elevated functional levels in this tissue. Mitochondrial-encoded COX2 mRNA levels were not limiting for functional activities in both tissues, in favour of post-transcriptional control or limitations by other transcripts of the COX complex. Altogether,the differentiation in gene expression between both populations was more strongly expressed at 4°C. The comparison of functional levels and transcript levels may reflect genetic differentiation at functional sites, in line with genetic differences between the two populations previously established by non-coding genetic markers.