Print PageAnimals with distinct life-stages are confronted with different parasites when larvae or adults. These different communities of parasites should exert different selective pressures on larval and adult immune defenses, therefore inducing the evolution of different investment into immune function at the different life-stages. However, if the immune systems of larvae and adults share the same genetic architecture, then their evolution cannot be independent. We investigated the, thus-far unexplored, genetic links between larval and adult immune system functioning using controlled crosses of Drosophila melanogaster. As a proxy for investment into immunity we monitored the constitutive transcription of 2 genes coding for antimicrobial peptides, Diptericin and Drosomycin. The products of these genes are directly active against pathogenic microbes.
Results/Conclusions
Larval and adult expression of Diptericin shared the same genetic architecture as revealed by a strong, positive genetic correlation between these traits. This contrasted with Drosomycin expression, where larval transcription was highly variable but adult transcription genetically invariant. The potential response to selection was higher for Drosomycin than for Diptericin as the expression of the latter gene was mostly determined by non-additive factors. We found no evidence for a fitness cost for the transcription of these genes in our study. To conclude, genetic correlations between larval and adult immunities imply that parasite pressure on one life-stage can drive the evolution of immunity (and resistance) in the other life-stage. Because immunity determines parasite success for infection and transmission, the coupled evolution of larval and adult immunities should link the dynamics of their specific communities of pathogens.
