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Eberhart, Johann
E-mail: eberhart@mail.utexas.edu Website: http://www.sbs.utexas.edu/eberhart Main Office: PAT 528 Alternate Office: PAT 517 Mailing Address: |
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Graduate Students: Research Summary: Craniofacial disease is common in humans because of the complexity of craniofacial development. This complexity is caused by the wide variety of cellular processes, including cell migration and cell signaling, necessary for proper craniofacial development. Much of the craniofacial skeleton derives from cranial neural crest cells, which emigrate from the dorsal neural tube and migrate along highly stereotyped pathways to the pharyngeal arches. In the first pharyngeal arch, neural crest cells that will populate anterior craniofacial regions, such as the palatal skeleton, associate intimately with the oral ectoderm. Our research on the Platelet-derived growth factor (Pdgf) and Sonic Hedgehog (Shh) signaling pathways in zebrafish shows reciprocal signaling between neural crest and the oral ectoderm guide development of the anterior craniofacial skeleton. Absence of either Pdgf or Shh signaling causes loss of both the palatal skeleton and regulatory gene expression in the oral ectoderm. Time lapse movies and genetic mosaic analyses show that neural crest cells require reception of Pdgf signaling to migrate to the oral ectoderm. The loss of oral ectodermal gene expression in the absence of Pdgf signaling is due to the loss of crest cells reaching the oral ectoderm, demonstrating the existence of a signal from the neural crest to the oral ectoderm. On the other hand, in the absence of Shh signaling, neural crest cells migrate to the oral ectoderm appropriately but are not stabilized and eventually move posterior to the eye. It is the oral ectoderm must receive Shh signaling to stabilize crest, thus implying a signal from the oral ectoderm to neural crest. We are currently using techniques such as transgenesis, time-lapse confocal microscopy and transplantation to determine the nature of these reciprocal signals. To broaden our understanding of cell signaling and other cellular processes governing anterior craniofacial development, we are analyzing zebrafish mutants with disruptions to specific craniofacial regions isolated in our forward genetic screen. Phenotypic characterization and genetic identification of these mutants will greatly expand our knowledge of the genetic networks underlying normal craniofacial development and human disease. Research Images:
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