Meeting Abstract
The physiological and regulatory processes that maintain energy homeostasis may provide stability in metabolic trajectories despite underlying genetic variation in populations. However, at present, we lack a detailed understanding of the links between genome variation, mitochondrial energetics and organismal metabolic rate. Here, we tested whether metabolic strategies in the fruit fly Drosophila melanogaster varied among genotypes and across ontogeny for both wildtype and mitochondrial-nuclear genotypes that have compromised mitochondrial oxidative phosphorylation (OXPHOS). We found that the fundamental scaling relationship between mass and metabolic rate differed significantly across development in Drosophila. There was a switch in metabolic scaling from hypermetric scaling in first instars to hypometric scaling in third instars. We also observed that mitochondrial respiration was maintained in second- and third-instars at similar levels, despite a significant increase in oxidative capacity per unit of mitochondrial protein during development. Furthermore, we found that genotypes differentiated into two groups—those that switch to mitochondrial ATP production before the second instar and those that continue relying on glycolytic ATP through the second instar. Interestingly, the mitochondrial-nuclear genotype with compromised OXPHOS had compensatory up-regulation of both glycolytic flux and oxidative capacity of mitochondria. This up-regulation was coincident with increased ROS production during the second instar and reduced mitochondrial membrane potential compared to other genotypes. Taken together, the data reveal that genetic defects in core physiology can be buffered at the organismal level and that there may be multiple genotypic and physiological paths to equivalent organismal outcomes within populations.
