Evolutionary and Molecular Determinants of a Nutritional Polyphenism

ongoing

Environmental fluctuations are a general challenge for organisms, exacerbated in the context of global change. Many animals evolve phenotypically plastic responses to adjust to new conditions. Polyphenism is an original mechanism that produces specialized morphs to track environmental changes. Whether the molecular mechanisms underlying polyphenism evolve from the acquisition of novel genes or the rewiring of conserved environment-sensing pathways is an unresolved and challenging question as it requires well-characterized regulatory networks, including the involvement of host-microbiota molecular interactions, and relevant phylogenetic frameworks to root the evolutionary steps through which polyphenism emerged. ALTEREVO aims to understand how a nutrient-sensitive polyphenism evolves and is regulated. It uses aphids and their symbionts, to characterize the molecular regulation of nutritional polyphenism, which induces alternative morphs adapted to distinct host plants, and to elucidate how this polyphenism machinery became genetically encoded. It also addresses for the first time the role of symbionts on the evolution and regulation of animal polyphenisms. To fulfil these objectives, ALTEREVO proposes an original approach linking the evolutionary, molecular and ecological components of polyphenism, and incorporating the involvement of symbionts. It relies on metabolomics to identify plant compounds inducing alternative phenotypes, large-scale gene expression and epigenetic analyses to reveal the molecular cascade regulating morph determination, functional characterization of candidate genes, and phylogenomics to elucidate nutritional polyphenism evolution. This project will lead major progress on the mechanisms allowing rapid phenotypic adjustments to environment fluctuations and on the role of phenotypic plasticity in evolution in a holobiont context. These advances are of fundamental importance for assessing the resilience of populations to human-induced changes.