Energetic stress and infection generate immunity-fecundity tradeoffs in Drosophila

Abstract

Physiological responses to short-term environmental stress, such as infection, can have long-term consequences for fitness, particularly if the responses are inappropriate or nutrient resources are limited. Genetic variation affecting energy acquisition, storage, and usage can limit cellular energy availability and may influence resource-allocation tradeoffs even when environmental nutrients are plentiful. Here, we utilize well-characterized Drosophila mitochondrial-nuclear genotypes to test whether disrupted energy metabolism interferes with nutrient-sensing pathways, and whether this disruption has consequences for tradeoffs between immunity and fecundity. We find that this energetically compromised genotype is resistant to rapamycin - a drug that stimulates nutrient-sensing pathways that are activated when resources are limited. Resource limitation also compromises survival in energetically-compromised genotypes, suggesting that this genotype may have little excess energetic capacity and fewer cellular nutrients, even when environmental nutrients are not limiting. Accordingly, we find that immune function is compromised in this genotype, but only in females, and that these females experience immunity-fecundity tradeoffs that are not evident in genotypic controls with normal energy metabolism. Thus, genetic variation in energy metabolism may act to limit the resources available for allocation to life-history traits in ways that generate tradeoffs even when environmental resources are not limiting.