TGIP · Trans-generational immune priming: molecular basis and fitness consequences

Trans-generational immune priming: molecular basis and fitness consequences

In the face of rapid ongoing environmental changes currently experienced by species, the survival of species is challenged. The belief that species potential to adapt to a changing environment relies solely on their genetic diversity and demography is been questioned by phenotypic plasticity. More recently, the discovery of environment-sensitive molecular processes that accelerate phenotypic variation opened new research avenues. Although the view that these non-genetic components may control species adaptive capacity is vigorously debated, if even partly true, could have profound implications for understanding species adaptive potential. Epigenetic components constitute important environment-sensitive mechanisms possibly accelerating responses to selective pressures. Even though there are several epigenetic pathways that can facilitate phenotypic plasticity, the addition of a methyl group to cytosine nucleotides in genes’ promoters is probably the best characterized to date. An emerging threat from globalization to species is the uncontrolled spread of parasites and diseases. Parasites alter a host’s fitness, influence populations, communities and ultimately ecosystem functions. Therefore, understanding the mechanisms of host’s resistance to pathogens is crucial. Importantly, at birth, where individuals mostly experience the same pathogenic environment as that of their parents, developing a rapid system for the transmission of labile resistance would appear beneficial. Thus far, the idea that mothers can alter offspring immune response and resistance via the transfer of immune cells either through the egg yolk or the placenta is widely accepted. Recently, scientists proposed that males may also contribute to offspring parasite resistance beyond the simple transfer of genetic material, also referred as paternal effects. But to what extend these effects alter the outcome of ecological interactions, such as hosts' parasite resistance is far from clear. Furthermore, their underlying mechanism remains poorly understood. By conducting a control infection experiment, we showed that paternal effects on parasite resistance exist. Most importantly, we provide evidence that the underlying mechanism of the trans-generational immune priming is DNA-methylation and modifications that are induced by the parasites can be transmitted across generations. This provides a fast way for offspring to effectively react to pathogens experienced from their parents.

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