Parasites are a major evolutionary force, driving adaptive responses in host populations. Although the link between phenotypic response to parasite-mediated natural selection and the underlying genetic architecture often remains obscure, this link is crucial for understanding the evolution of resistance and predicting associated allele frequency changes in the population. To close this gap, we monitored the response to selection during epidemics of a virulent bacterial pathogen, Pasteuria ramosa, in a natural host population of Daphnia magna. Across two epidemics, we observed a strong increase in the proportion of resistant phenotypes as the epidemics progressed. Field and laboratory experiments confirmed that this increase in resistance was caused by selection from the local parasite. Using a genome wide association study (GWAS), we built a genetic model in which two genomic regions with dominance and epistasis control resistance polymorphism in the host. We verified this model by selfing host genotypes with different resistance phenotypes and scoring their F1 for segregation of resistance and associated genetic markers. Such epistatic effects with strong fitness consequences in host-parasite coevolution are believed to be crucial in the Red Queen model for the evolution of genetic recombination.

Dietary restriction (DR) is the most consistent environmental manipulation to extend lifespan. Originally thought to be caused by a reduction in caloric intake, recent evidence suggests that macronutrient intake underpins the effect of DR. The prevailing evolutionary explanations for the DR response are conceptualized under the caloric restriction paradigm, necessitating reconsideration of how or whether these evolutionary explanations fit this macronutrient perspective. In the authors’ opinion, none of the current evolutionary explanations of DR adequately explain the intricacies of observed results; instead a context‐dependent combination of these theories is suggested which is likely to reflect reality. In reviewing the field, it is proposed that the ability to track the destination of different macronutrients within the body will be key to establishing the relative roles of the competing theories. Understanding the evolution of the DR response and its ecological relevance is critical to understanding variation in DR responses and their relevance outside laboratory environments.

Dietary restriction (DR), limiting calories or specific nutrients without malnutrition, extends lifespan across diverse taxa. Traditionally, this lifespan extension has been explained as a result of diet‐mediated changes in the trade‐off between lifespan and reproduction, with survival favored when resources are scarce. However, a recently proposed alternative suggests that the selective benefit of the response to DR is the maintenance of reproduction. This hypothesis predicts that lifespan extension is a side effect of benign laboratory conditions, and DR individuals would be frailer and unable to deal with additional stressors, and thus lifespan extension should disappear under more stressful conditions. We tested this by rearing outbred female fruit flies (Drosophila melanogaster) on 10 different protein:carbohydrate diets. Flies were either infected with a bacterial pathogen (Pseudomonas entomophila), injured with a sterile pinprick, or unstressed. We monitored lifespan, fecundity, and measures of aging. DR extended lifespan and reduced reproduction irrespective of injury and infection. Infected flies on lower protein diets had particularly poor survival. Exposure to infection and injury did not substantially alter the relationship between diet and aging patterns. These results do not provide support for lifespan extension under DR being a side effect of benign laboratory conditions.

9Dietary restriction (DR), limiting calories or specific nutrients, extends lifespan across 10 diverse taxa. This lifespan extension has been explained as diet-mediated changes in the trade-11 off between lifespan and reproduction, with survival favoured with scarce resources. Another 12 evolutionary hypothesis suggests the selective benefit of the response is the maintenance of 13 reproduction. This hypothesis predicts that lifespan extension is a side effect of benign 14 laboratory conditions, where DR individuals are frailer and unable to deal with additional 15 stressors, and thus lifespan extension should disappear under more stressful conditions. We 16 tested this by rearing outbred female Drosophila melanogaster on 10 different 17 protein:carbohydrate diets. Flies were either infected with a bacterial pathogen (Pseudomonas 18 entomophila), injured or unstressed. We monitored lifespan, fecundity and ageing measures. 19 DR extended lifespan and reduced reproduction irrespective of injury and infection. These 20 results do not support lifespan extension under DR being a side effect of benign laboratory 21 conditions. 22 23