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Our laboratory studies growth factor signaling pathways that have important roles in mouse craniofacial and early embryonic development. In particular, our lab is interested in the general question of how biological specificity is acquired upon engagement of growth factor signaling. We are in the Departments of Developmental and Regenerative Biology and Oncological Sciences at Mt. Sinai School of Medicine, and our laboratory is on the 25th Floor of the Annenberg Research Building (large black building on the left), overlooking Central Park. Projects currently underway are summarized below.

Platelet derived growth factor (PDGF) signaling is critical for normal developmental processes. PDGFs regulate the development of a variety of mesenchymal stem cells, including cranial neural crest cells, vascular smooth muscle cells and pericytes. To determine the role of signal transduction pathways that operate in the PDGF signaling pathway, we have created allelic series at both PDGF receptor loci carrying specific point mutations that prevent docking of effector proteins to the receptors. We are presently focusing our efforts on understanding the pathways by which PDGF signaling regulates the development of the midface and palate. In addition, we have generated activating, ligand-independent mutations in PDGF receptors that identified important roles for this signaling pathway in fibrosis, cancer and differentiation of mesenchymal stem cells. We have identified mediators of PDGF signaling and shown that they operate in the PDGF pathway, using a platform in which gene trap mutagenesis is coupled to DNA microarrays. We are also using a gene trap approach combined with somatic transposon mutagenesis to identify factors that cooperate with PDGF in glioma progression.

Fibroblast growth factor (FGF) signaling plays pivotal roles in physiological processes and in embryonic development, particularly in mesoderm and craniofacial development, and in the formation of extraembryonic tissues required for survival and proper patterning of the embryo. We are generating point mutations in the two essential FGF receptors, to identify critical signaling pathways that operate during craniofacial development and in the establishment of extraembryonic stem cells.

Eph receptors and ephrins function as receptor/ ligand pair that act in axon guidance and in establishing boundaries during embryonic development. This signaling pathway is unusual as ephrins can activate both forward signaling to Eph receptors as well as reverse signaling through their GPI-anchor or cytoplasmic domain. We are studying the signaling pathways through which ephrin-B1 regulates cranial neural crest development and ephrin- B2 regulates trunk neural crest development. By integrating phospho-proteomic and transcriptomic approaches, we have recently identified cell proliferation as a novel mechanism by which Eph/ephrin signaling controls craniofacial development.