Abstract
Mitochondrial oxidative phosphorylation provides over 90% of the energy produced by aerobic organisms, therefore the regulation of mitochondrial activity is a major issue for coping with the changing environment and energy needs. In fish, there is a large body of evidence of adaptive changes in enzymatic activities of the OXPHOS pathway, but less is known at the transcriptional level and the first aim of the present study was to define the molecular identity of the actively transcribed subunits of the mitochondrial respiratory chain of a livestock animal, using gilthead sea bream as a model of farmed fish with a high added value for European aquaculture. Extensive BLAST searches in our transcriptomic database (www.nutrigroup-iats.org/seabreamdb) yielded 97 new sequences with a high coverage of catalytic, regulatory and assembly factors of Complex I to V. This was the basis for the development of a PCR array for the simultaneous profiling of 88 selected genes. This new genomic resource allowed the differential gene expression of liver and muscle tissues in a model of 10 fasting days. A consistent down-regulated response involving 72 genes was made by the liver, whereas an up-regulated response with 29 and 10 differentially expressed genes was found in white skeletal muscle and heart, respectively. This differential regulation was mostly mediated by nuclear-encoded genes (skeletal muscle) or both mitochondrial- and nuclear-encoded genes (liver, heart), which is indicative of a complex and differential regulation of mitochondrial and nuclear genomes, according to the changes in the lipogenic activity of liver and the oxidative capacity of glycolytic and highly oxidative muscle tissues. These insights contribute to the identification of the most responsive elements of OXPHOS in each tissue, which is of relevance for the appropriate gene targeting of nutritional and/or environmental metabolic disturbances in livestock animals.
Highlights
The main cellular function of mitochondria is the production of ATP by oxidation of metabolic fuels in the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS) pathway
NADH and FADH2 function as electron donors of Complex I (NADH: ubiquinone oxidoreductase) and Complex II that are transported through Complex III to Complex IV, where molecular oxygen serves as the final electron acceptor of the mitochondrial respiratory chain
White skeletal muscle and heart gene expression are shown in S11 Table
Summary
The main cellular function of mitochondria is the production of ATP by oxidation of metabolic fuels in the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS) pathway. In this process, NADH and FADH2 function as electron donors of Complex I (NADH: ubiquinone oxidoreductase) and Complex II (succinate dehydrogenase) that are transported through Complex III (ubiquinol cytochrome c reductase) to Complex IV (cytochrome c oxidase), where molecular oxygen serves as the final electron acceptor of the mitochondrial respiratory chain. All this is encompassed by a complex regulation of nuclear and mitochondrial genomes, which involves hundreds of genes controlling the expression, function, transport, assembly and turnover of mitochondrial proteins and enzyme subunits of OXPHOS in particular [3]
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