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 targeted and conditional gene disruption in mice, we generate mice harboring targeted point mutations that disrupt specific signal transduction pathways. By integrating these in-vivo approaches with embryo culture, live imaging, mass spectrometry-based phospho-proteomics, cell biology and biochemistry, we seek to understand the mechanistic basis of signaling control of craniofacial development.
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 (2012) Eph/ephrin signaling: Genetic, phosphoproteomic, and transcriptomic approaches. Seminars in cell & developmental biology, 23(1):26-34. PubMed
Bush, J.O. and R. Jiang, R.(2011) Palatogenesis: morphogenetic and molecular mechanisms of secondary palate development. Development 139(2): 231-43. 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