Meeting Abstract
S2-2.4 Jan. 4 Trunk neural crest cells contribute to plastron and nuchal bones in turtles GILBERT, S.F.*; BENDER, G.; YIN, M.; CEBRA-THOMAS, J. A. ; Swarthmore College; Swarthmore College; Swarthmore College; Millersville University sgilber1@swarthmore.edu
The plastron of the hard-shelled turtle Trachemys scripta contains nine bones. These bones develop by intramembranous ossification within the dermis. The three anterior plastral bones (the paired epiplastra and the endoplastron) are thought to be homologues of the clavicles and intraclavicular bone, respectively; while the remaining three pairs of plastron bones are believed to be homologous to gastralia (floating ribs) of other reptiles. The plastron bones have two distinct phases of development. In the first phase, a band of cells condenses to form an aggregate, while in the second stage, these aggregates form bony matrix. A similar pattern is seen in the nuchal bone, the most anterior bone in the carapace. Our studies provide evidence that the plastral and nuchal bones are each derived from trunk neural crest cells. We show that the cells forming these bones stain positively for HNK-1, FoxD3, p75, and the alpha subunit of the platelet-derived growth factor receptor. Each of these antigens is a marker for skeletogenic neural crest cells. These plastron-forming cells appear to be a late-migrating population of neural crest cells, emerging from the neural tube at stage 17, more than a week after the other neural crest cells have left. We have shown by DiI labeling that this is a migratory cell population. In addition, we demonstrate that the gastralia of the alligator also stains positively for HNK-1. These studies show that the turtle trunk neural crest is capable of naturally forming dermal skeleton, and that the plastral bones form in the same manner as the facial bones. It is possible that to become skeletogenic, these neural crest cells must either lose posterior Hox gene expression and/or be placed in an environment that will support skeletogenic gene expression.