Meeting Abstract
Phenotypic plasticity has been heralded as an essential mechanism for surviving climate change and an important consideration in speciation. Since plasticity is likely to enable expansion and radiation into new environments, it has hypothesized to be an ancestral trait that is then lost as the new populations become specialized. Less clear, is how and when plasticity arises. A phenotypic response to an external cue starts with translation of the environment, often by neurosensation. Genes that encode components of neurosensory systems, such as sensory receptors, are known to undergo rapid radiations, with both duplications and losses that allow for niche expansion and host shifts. I hypothesize that the evolvability of neurosensory systems controls the gain and loss of phenotypic plasticity. To test this hypothesis, I surveyed Echinoidea for pre-feeding plasticity in arm length in response to food availability and for the underlying neurosensory mechanism. Many echinoids can inhibit elongation of their feeding arms via food-induced dopamine signaling during development. My data suggest that pre-feeding plasticity arose in the regular urchins, with numerous subsequent losses within this clade. These losses appear to have been driven by 1) temporal shifts in the development of catecholaminergic neurons and 2) changes in expression or function of sensory components – supporting my hypothesis. The establishment of the developmental response may have been constrained by the temporal alignment of neural development and skeletal development. Since TGF-β signaling mediates both neurogenesis and skeletal development, the pleiotropic effects underlying the heterochronic shift in skeletogenesis may have initially inhibited catecholaminergic neural development.
