Meeting Abstract

P2.179  Monday, Jan. 5  Inhibition of the canonical Wnt signaling pathway during craniofacial development: impact on the craniofacial phenotype of Xenopus tadpoles DESCAMPS, E*; VLEMINCKX, K; ADRIAENS, D; Ghent University, Belgium; Flanders Flanders Interuniversity Institute for Biotechnology, Belgium; Ghent University, Belgium Emilie.Descamps@UGent.be

The head is anatomically the most complex part of the body. Given the complexity of the craniofacial structures, many genes and embryonic tissue sources are known to be involved in their ontogeny. Among other processes, Wnt proteins are implicated in the induction and differentiation of neural crest cells. These cells give rise to most of the craniofacial skeleton and to the peripheral nervous system. As such, many craniofacial defects may originate from abnormal regulation of Wnt signals. We want to examine the implications of the postembryonic Wnt activity in the Xenopus head. Therefore, we tested to what degree inducibly inactivating the canonical Wnt signaling pathway during early development results in skeletal deformations of the cartilaginous skull. Additionally, relations between abnormal development of the central nervous system and the architecture of the cartilaginous brain-case are studied. Our focus lies on two particular aspects: the macro-anatomy of the brain and the craniofacial skeleton. Comparison of the head morphology and histology between wild-type and transgenic tadpoles allows us to investigate and describe the variation of the craniofacial structures, as well as the brain anatomy. Transgenic stage 40 tadpoles were exposed to dexamethasone, activating an inducible Wnt-inhibiting chimeric transgene, and fixed at stage 46. Serial histological sectioning of the craniofacial region was performed. Detailed anatomical 3D analysis of the craniofacial region in the wild-type and the transgenic model organism at stage 46 were carried out, and compared to the wild-type stage 40 phenotype. We aim to find out what modifications are linked to inactivating the Wnt signaling pathway, and to what degree the observed phenotypes reflect a constancy.