To accommodate the stress induced by climate change, aquatic organisms face the choice of either moving to a better environment or adapting to changes. However, life history trade-offs limit the effectiveness of adaptation. Parasites and pathogens are widespread and exert strong selection pressure. Indirect changes in environmental salinity can impact immune defences and the survival of populations in their current environment. Adapting to salinity reduces the ability to respond to other challenges like parasites and diseases, which can disrupt immune functions and related genes.
Parasites play a role in evolution by promoting the fight against diseases in multiple manners, including tolerance. Tolerance enables hosts to endure infections without significant negative effects on their fitness and unlike resistance does not lead to the elimination of the parasites. Yet, the underlying mechanisms and possible heritability of this mechanisms remain unknown. In certain fish species, paternal infection is linked to increased disease tolerance in offspring, and infection is associated with DNA methylation. However, the precise role of DNA methylation in transmitting tolerance remains to be evidenced.
The primary objectives of our research were to:
1. Describe the methylation patterns related to immunity and salinity.
2. Identify genes involved in the trade-off of methylation between immunity and salinity.
3. Experimentally examine the induction of trade-offs through changes in salinity and parasite infection.
4. Functionally test the effects of methylation trade-offs on gene expression.
DNA methylation, an important epigenetic marks, plays a crucial role in understanding its transmission mechanisms and trade-offs among different stressors. This knowledge is essential in the fields of evolutionary biology and biodiversity conservation. Additionally, DNA methylation has been observed to change in relation to factors like age and cancer type, making our research relevant to various areas of biomedicine with potential significant implications.
We found a strong correlation between the infectious status of fathers and changes in the methylome of their offspring. This effect was so strong that the offspring infection status hardly predicted their methylation patterns compared to that of their father. Ultimately, we identified DNA methylation marks that were associated with tolerance, that could be used as potential biomarkers. Our results provide new insights into the molecular mechanisms underlying tolerance as well and trans-generational immune priming via the paternal line.
