Abstract
Heritable population differences in immune gene expression following infection can reveal mechanisms of host immune evolution. We compared gene expression in infected and uninfected threespine stickleback (Gasterosteus aculeatus) from two natural populations that differ in resistance to a native cestode parasite, Schistocephalus solidus. Genes in both the innate and adaptive immune system were differentially expressed as a function of host population, infection status, and their interaction. These genes were enriched for loci controlling immune functions known to differ between host populations or in response to infection. Coexpression network analysis identified two distinct processes contributing to resistance: parasite survival and suppression of growth. Comparing networks between populations showed resistant fish have a dynamic expression profile while susceptible fish are static. In summary, recent evolutionary divergence between two vertebrate populations has generated population-specific gene expression responses to parasite infection, affecting parasite establishment and growth.
Highlights
Helminths are a diverse group of parasitic worms, which often establish long lasting infections in their vertebrate hosts [1], despite host immune activity
Using a large scale controlled laboratory infection experiment, we find changes in gene expression between two host populations, and as a function of infection status
Our analysis suggests that host resistance involved two components; response to challenge by cestodes, and control over cestode growth
Summary
Helminths are a diverse group of parasitic worms, which often establish long lasting infections in their vertebrate hosts [1], despite host immune activity. Host resistance depends on a complex signaling cascade, starting with the detection of pathogen molecules or pathogen induced damage to host tissues, followed by activation of a diverse suite of innate and adaptive immune cell populations. A key question in biology is, why does parasite resistance differ among host individuals or populations? These cells may proliferate, migrate, or produce molecules that signal to other immune cells or directly attack the parasite. Natural genetic variation in host resistance could arise from any stage(s) in an immune cascade
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