Research Interests

Congenital anomalies occur in 1% of all live human births. Approximately one third of these developmental anomalies affect craniofacial development, which depends upon multipotent neural crest cells. Neural crest cells are induced in the neuroepithelium and migrate throughout the body where they differentiate into a variety of tissues such as craniofacial bone, cartilage and connective tissue, as well as neurons and glia of the peripheral nervous system and pigment cells in the skin. Depending on the stage and axial level of the disruption in neural crest cell development, distinct phenotypes of the craniofacial, cardiac or enteric nervous system tissue occur. Therefore, it’s important to understand the mechanisms that regulate neural crest cell development. 
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Mediator complex and craniofacial development
The Mediator complex is a multiprotein complex that forms a molecular bridge between RNA polymerase II and transcription factors and thus is required in all cells for RNA polymerase II driven transcription. I have observed that a point mutation in a tail Mediator complex subunit Med23 results in severe craniofacial malformations that arise from defects in neural crest development. This raises the question of how disruptions in a ubiquitously expressed gene and a global process results in tissue specific defects. Our findings demonstrate a link between the global transcriptional machinery and developmental signaling pathways that elicit tissue specific effects in development and disease. Future research in Dash Lab is focused on parsing the function of individual Mediator complex subunits in craniofacial development and congenital disorders.