Poster Sessions

DEV-16

Diane Adams

D. Adams, L. Angerer

Dopamine Mediates Ectodermal-Mesenchymal Signaling Underlying a Developmental Response to Food Availability

Embryonic processes are often considered as scripted readouts of robust developmental programs largely independent of environmental inputs. However, development can also be plastic, dependent on the environmental context. Many human diseases and developmental defects are believed to result from complex interactions between genetic predisposition and the environment. Sea urchin larvae provide a classic example of developmental plasticity in which to study how environmental factors can be incorporated into normal developmental programs. For example, pre-feeding sea urchin larvae alter the development of their feeding apparatus in response to food availability to optimize expected food intake versus expenditure of maternal energetic stores. Since they do not yet feed, larvae perceive food concentration through chemosensation and mechanosensation. We hypothesize that sensors in the arms of pre-feeding sea urchin larvae can initiate ectoderm/mesenchyme signaling to adjust the size of the feeding apparatus (length of arms). A screen of pharmaceuticals targeted to known sea urchin neurotransmitters revealed that dopaminergic neurons are involved in regulating arm growth in pre-feeding larvae of Stronglyocentrotus purpuratus. Immunofluorescent staining for dopamine and tyrosine hydroxylase, the rate limiting enzyme in dopamine biosynthesis, revealed dopaminergic neurons at the tips of the post-oral arms, within and basal to the ciliary band, and immediately adjacent to the skeletal mesenchyme. Thus, dopaminergic neurons are placed correctly to mediate the ectodermal-mesenchymal signaling underlying the developmental response. Pharmacological perturbation of dopamine D2 receptor function recapitulated phenotypic differences observed in larvae reared in high and no/low food treatments. In larvae exposed to the dopaminergic D2 receptor antagonist, Amisulpride, the post-oral rods were significantly longer than those in control larvae and the drug treatment obliterated the phenotypic response to food. In contrast, in larvae exposed to the dopaminergic D2 receptor agonist, Quinpirole, the rods were shorter than in control larvae, recapitulating the phenotypic response to food. We propose that food sensation induces the release of dopamine which inhibits skeletal mineralization and cell proliferation in the larval arms. Our data demonstrate environmental regulation of embryonic development via a neurochemical signal.