Immune-Energetic Interactions in Mitochondrial-Nuclear Hybrids
An organism's energy availability is often determined by nutrients in the environment, and the dynamic allocation of these resources within the lifespan of an individual impacts life-history trade-offs between organismal maintenance and reproduction. Life-history trade-offs can vary between individuals within a species or within an individual across life stages, and be impacted by responses to environmental stress, such as the immune response. One regulatory mechanism underlying these trade-offs is the target of rapamycin (TOR) signaling pathway, which balances between protein production and autophagy. To investigate the role of energetics and autophagy in mediating immune fuction and trade-offs between immune function and life-history traits, such as fecundity, I use a set of mitochondrial-nuclear, D. melanogaster and D. simulans, hybrid genotypes. One of these genotypes, (simw501);OreR, has compromised oxidative phosphorylation activity, which is essential for ATP production. This causes decreased female fecundity, delayed development time, and disrupted larval metabolic rate, which is indicative of inefficient energy metabolism. This genotype and its compatible mitochondrial-nuclear genotypic controls provide a powerful tool for investigating the consequences of energy allocation without changing nutrient availability via diet. These experiments test the hypothesis that effective immune responses require significant energetic investment. I predict that (simw501);OreR Drosophila larvae (1) intrinsically compensate for their inefficient energy metabolism by activating autophagy and (2) mount less effective immune responses in response to bacterial infection.