Meeting Abstract
The origin of the turtle shell over 200 million years ago greatly modified the amniote body plan, and the morphological plasticity of the shell has promoted the adaptive radiation of turtles. The shell is a layered structure formed by basal endochondral axial skeletal elements (ribs, vertebrae) and plates of bone, which are overlain by keratinous ectodermal scutes. Scutes develop as ectodermal appendages from placodal signaling centers and are patterned by reaction-diffusion dynamics. These placodal signaling centers are hypothesized to be developmental modules that are responsible for the evolutionary plasticity and diversification of the turtle shell’s scute patterns. A computational model shows how two coupled reaction-diffusion systems reproduce both natural and abnormal variation in turtle scutes, and hypothesizes that scute anomalies are epigenetic and may be a consequence of environmental conditions during incubation. Corroborating this hypothesis is evidence from natural nests of cheloniid sea turtles that were incubated under natural conditions, but during normal and hotter-than normal years. We observe that scute anomalies increase greatly in hot conditions and increase further with drought. We further examine scute variation by systematically introducing different perturbations of different magnitudes and at different stages into in silico scute development, thereby characterizing and quantifying the variation generated epigenetically over development. This way, we draw a variational morphospace that might provide insight into the developmental origin of phenotypic variation.
