Data from: The complex contributions of genetics and nutrition to immunity in Drosophila melanogaster

Both malnutrition and undernutrition can lead to compromised immune
defense in a diversity of animals, and “nutritional immunology” has been
suggested as a means of understanding immunity and determining strategies
for fighting infection. The genetic basis for the effects of diet on
immunity, however, has been largely unknown. In the present study, we have
conducted genome-wide association mapping in Drosophila melanogaster to
identify the genetic basis for individual variation in resistance, and for
variation in immunological sensitivity to diet (genotype-by-environment
interaction, or GxE). D. melanogaster were reared for several generations
on either high-glucose or low-glucose diets and then infected with
Providencia rettgeri, a natural bacterial pathogen of D. melanogaster.
Systemic pathogen load was measured at the peak of infection intensity,
and several indicators of nutritional status were taken from uninfected
flies reared on each diet. We find that dietary glucose level
significantly alters the quality of immune defense, with elevated dietary
glucose resulting in higher pathogen loads. The quality of immune defense
is genetically variable within the sampled population, and we find genetic
variation for immunological sensitivity to dietary glucose
(genotype-by-diet interaction). Immune defense was genetically correlated
with indicators of metabolic status in flies reared on the high-glucose
diet, and we identified multiple genes that explain variation in immune
defense, including several that have not been previously implicated in
immune response but which are confirmed to alter pathogen load after RNAi
knockdown. Our findings emphasize the importance of dietary composition to
immune defense and reveal genes outside the conventional “immune system”
that can be important in determining susceptibility to infection.
Functional variation in these genes is segregating in a natural
population, providing the substrate for evolutionary response to pathogen
pressure in the context of nutritional environment.