Dr. Rogers’ research focuses on development of the craniofacial complex, -- chiefly the skull, cranial base, lip and palate -- and seeks to discover how craniofacial anomalies including cleft lip and palate and craniosynostosis arise during embryogenesis . Her work addresses these questions through a combination of classical embryology and cell biological techniques and encompasses the following areas:
Developmental etiology including molecular and cellular mechanisms in the development of orofacial clefting
Using mouse models, Dr. Rogers and colleagues are working to understand development of cleft lip and palate. Dr. Rogers hypothesizes that in the developing face, an appropriate merging of skeletogenic condensations must occur in the frontonasal process and cranial base. In several mouse models, Dr. Rogers and her research team have observed defects in midline merging. They are working to determine the genetic and mechanistic defects underlying these defects – testing whether they arise from increased proliferation, decreased cell death and/or from changes in signaling that prevent condensations from merging. Dr. Rogers’ expects the data to identify novel mechanisms and genes that contribute to orofacial clefting.
Control and development of the skull vault and cranial base
Skull vault and cranial base mineralization and maturation are intriguing because of the former’s process of intramembraneous ossification and the latter’s endochondral ossification. Both of these structures are of composite cell origin, with the more anterior regions being derived from the neural crest and the more posterior being developed from mesoderm.
Dr. Rogers and colleagues have observed significant defects in the heads of Beetlejuice mutants, which have a missense mutation in Prickle1. Prickle1 is a core component of the Wnt/planar cell polarity pathway. The Wnt/PCP pathway polarizes cytoplasmic constituents and enables for asymmetric secretion and division. An open question in the field is how these processes contribute to normal and abnormal craniofacial development and, in particular, how the development of the neural crest-derived regions of the skull use this pathway in at least two phases of migration. Dr. Rogers’ lab is currently working to determine whether defective migration and/or differentiation cause the phenotypes seen in the Beetlejuice mutants.
Cell polarization and orientation functions in craniofacial development
Dr. Rogers and her team have recently shown that Dspp-/-enamel undergoes accelerated differentiation. Dspp is translated and transcribed as a pre-protein. Post-translation modification involves cleavage into two proteins—dentin phosphoprotein (Dpp) and dentin sialophosphoprotein (DSP). The Dspp-/- mice lack both of these proteins. In preliminary analysis, Dr. Rogers’ and her team have found that the odontoblast and osteoblasts have developmental effects. Current work in this area focuses on testing to determine if these defects arise from defects in polarization and orientation.