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Valdivieso, A.

Publications and source records attributed to Valdivieso, A..

3 recordsLinked to original sources

Decoupling epigenetic variation from genetic variation reveals complementary dimensions of coral eco-evolutionary dynamics

Understanding how intraspecific diversity is structured is essential for predicting the eco-evolutionary trajectories of populations, especially under rapid environmental change. While such diversity has been extensively studied from a genetic perspective, much less is known about the distribution and ecological relevance of epigenetic variation within natural populations. To address this question, we focused on two species of reef-building corals belonging to distinct functional groups, Pocillopora acuta and Acropora hyacinthus, sampled across the South Pacific (New Caledonia, Fiji, French Polynesia). Using genome-wide Enzyme-Methyl sequencing, we jointly analyzed genetic (SNPs) and DNA methylation (CpGs) variation, while explicitly disentangling genetically associated from genetically independent epigenetic variation. Genetic and epigenetic structure showed contrasting spatial patterns, reflecting distinct temporal and ecological components of population dynamics. Genetic structure was strongest between archipelagos and followed an isolation-by-distance pattern consistent with long-term evolutionary processes. In contrast, epigenetic variation converged between colonies from different archipelagos. At finer spatial scales within archipelago, genetically independent epigenetic variation exhibited stronger structure than both genetic and genetically associated epigenetic variation, likely reflecting local environmental conditions. Together, our results show that genetic and epigenetic variation provide complementary insights into the eco-evolutionary processes shaping intraspecific diversity.

evolutionary biology↗

Multi-Omics Reprogramming Drives a Counterintuitive Reversal of Disease Susceptibility During Ageing

Ageing is a progressive and irreversible biological process characterized by the deterioration of physiological functions and increased vulnerability to mortality. Although extensively studied in vertebrates, ageing in long-lived invertebrates remains comparatively unexplored. While ageing typically leads to greater susceptibility to infectious diseases, a striking and unexpected reversal was identified in oysters: older oysters exhibit markedly increased tolerance to the Pacific Oyster Mortality Syndrome (POMS), a panzootic disease primarily driven by the OsHV-1 herpesvirus and responsible for severe losses in global aquaculture. To investigate this counterintuitive pattern, we challenged oysters aged 4, 16, and 28 months from four biparental families and conducted an integrative multi-omics analysis, including epigenomics, transcriptomics, and metabolomics on the two families showing the strongest age-related increase in survival. Our results reveal that ageing in Magallana gigas is characterized by coordinated epigenetic, transcriptional, and metabolic reprogramming that reduces host permissiveness to POMS. We show that the epigenetic remodeling of key immune regulators (e.g., Toll-like receptors, MyD88) aligns with transcriptional rewiring of NF-{kappa}B and ubiquitin pathways, producing a finely tuned innate immune state marked by enhanced antiviral activity but reduced antibacterial responsiveness. We also identify age-related repression of mTOR signaling, likely promoting autophagy and improving viral control. These regulatory changes are tightly linked to metabolic adjustments, including reduced TCA cycle flux, remodeled nitrogen metabolism, and altered glutathione dynamics, which collectively support a stress-tolerant, energy-conserving phenotype. Together, our findings reveal a fundamental evolutionary trade-off: juveniles prioritize growth at the cost of viral susceptibility, whereas adults invest in cellular maintenance and antiviral preparedness.

genomics↗

Epigenetic then genetic variations underpin rapid adaptation of oyster populations (Crassostrea gigas) to Pacific Oyster Mortality Syndrome (POMS)

Disease emergence is accelerating in response to human activity-induced global changes. Understanding the mechanisms by which host populations can rapidly adapt to this threat will be crucial for developing future management practices. Pacific Oyster Mortality Syndrome (POMS) imposes a substantial and recurrent selective pressure on oyster populations (Crassostrea gigas). Rapid adaptation to this disease may arise through both genetic and epigenetic mechanisms. In this study, we used a combination of whole exome capture of bisulfite-converted DNA, next-generation sequencing, and (epi)genome-wide association mapping, to show that natural oyster populations differentially exposed to POMS displayed signatures of selection both in their genome (single nucleotide polymorphisms) and epigenome (CG-context DNA methylation). Consistent with higher resistance to POMS, the genes targeted by genetic and epigenetic variations were mainly related to host immunity. By combining correlation analyses, DNA methylation quantitative trait loci, and variance partitioning, we revealed that a third of the observed phenotypic variation was explained by interactions between the genetic sequence and epigenetic information, [~]14% by the genetic sequence, and up to 25% by the epigenome alone. Thus, as well as genetic adaptation, epigenetic mechanisms governing immune responses contribute significantly to the rapid adaptation of hosts to emerging infectious diseases.

evolutionary biology↗