Our lab studies basic mechanisms by which signaling between cells coordinates morphogenesis. Understanding this control has significance beyond its fundamental importance in development since birth defects are the leading cause of death for infants during the first year of life. Craniofacial anomalies are the most common class of congenital defect in humans, with three quarters of all malformations identified at birth involving craniofacial dysmorphogenesis. We utilize multiple approaches based in mouse genetics to understand fundamental signaling processes as they relate to craniofacial development and disease. In addition to mouse genetics approaches, we utilize human induced pluripotent stem cells and live imaging to understand the cellular and molecular control of morphogenesis.
Kim, S., Lewis A.E., Singh V., Ma, X., Adelstein, R., Bush, J.O.,* (2015) Convergence and extrusion are required for normal fusion of the mammalian secondary palate. PLOS Biology, 13(4) Pubmed
Agrawal, P., Wang, M., Kim, S., Lewis, A.E., Bush, J.O.* (2014) The embryonic expression of EphA receptor genes in mice supports their candidacy for involvement in cleft lip and palate. Developmental Dynamics, 243 (11): 1470-6. Pubmed
Lewis, A., Vasudevan, H., O’Neill, A., Soriano, P., Bush, J.O.* (2013)The widely used Wnt1-Cre transgene causes developmental phenotypes by ectopic activation of Wnt signaling. Developmental Biology, 379(2):229-34. PubMed.
Bush, J. O. and Soriano, P. (2010). Ephrin-B1 forward signaling regulates craniofacial morphogenesis by controlling cell proliferation across Eph-ephrin boundaries. Genes Dev. 24, 2048-60. PubMed
Bush, J. O. and Soriano, P. (2009). Ephrin-B1 regulates axon guidance by reverse signaling through a PDZ-dependent mechanism. Genes Dev. 23, 1586-99. COVER IMAGE. PubMed