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 a 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 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.
A paper entitled "Convergence and Extrusion Are Required for Normal Fusion of the Mammalian Secondary Palate" was published in the April edition of PLOS Biology. This work utilizes live imaging to understand the cellular mechanisms of tissue fusion in the developing secondary palate. It identifies convergence of the epithelium driven by actomyosin contractility and cellular extrusion as important and previously unappreciated drivers of this morphogenesis.
Puja Agrawal, an SRAI who started in the lab as a Berkeley undergraduate whas moved on to M.D. Ph.D.studies at the Medical College of Wisconsin.During Puja's time in the lab, she made major contributions to our studies o fEphA/ephrin-A signaling in craniofacial development and had a first-author publication on this topic.