Mechanisms and Costs of Adaptive Plasticity in a Starlet Anemone (Nematostella Vectensis) Model

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Adaptive plasticity arguably represents the best defense animals have against the mounting effects of climate change. However, stressor interactions can undermine this important defense. My research uses a bottom-up approach to identify the signaling pathways that regulate plastic responses to environmental stress in a starlet anemone (Nematostella vectensis) model. The proposed work also capitalizes on the clonal ability of N. vectensis to test whether plasticity carries inherent costs. My first objective seeks to identify the molecular pathways that regulate plastic responses to thermal, osmotic, hypoxic, and nutritional stress. Nuclear receptors (NRs) represent strong candidates to integrate environmental inputs with cellular responses because they function both as small molecule receptors and regulators of large-scale transcriptional networks. My lab will investigate three N. vectensis NRs: i) an ortholog of vertebrate hepatocyte nuclear factor 4a, ii) a cnidarian-specific retinoid X receptor subfamily member, and iii) a Tailles subfamily member. Importantly, these three NRs have been associated with plastic responses in a number of animal systems. Using custom transgenic lines for each of these NRs, my lab will test how their expression levels, DNA-binding dynamics, protein-interaction networks, and activity patterns respond to shifts in temperature, salinity, oxygenation, and nutrient availability. This objective co-opts my expertise in high-throughput drug screening - but to screen for environmental stressors instead. My second objective will use overlaps in signalling pathways (identified in objective 1) to predict stressor interactions that manifest ecological costs of plasticity. For example, if a given NR regulates responses to both thermal and osmotic stress, we would expect that certain temperature-salinity combinations could undermine plasticity. Thermal stress, for instance, might a) jam the signaling pathways that coordinate responses to osmotic stress, or b) induce a phenotype that has increased vulnerability to osmotic stress. By quantifying the capacity for plasticity in wild-collected genotypes and measuring physiological performance traits (i.e., metabolic rate, developmental rate, growth rate), my lab can test whether specific stressor interactions promote ecological costs. If there are ecological costs associated with plasticity, we would expect performance traits to be most disrupted in genotypes with the highest capacities for plasticity. Collectively, this program will help provide a predictive framework to model the ecological costs of plasticity - a goal that is increasingly critical with the effects of climate change. In addition to providing a more comprehensive understanding of NR signalling and evolution, this work will help identify novel barriers to climate change responses and help determine whether plasticity will be enough to overcome the increasingly complex and rapid changes in environment animals face.