A postdoctoral fellow is needed to work on identifying signaling mechanisms promoted by Fgfr1 and Fgfr2 in craniofacial development. We have previously generated allelic series of point mutations at the Fgfr1 and Fgfr2 loci that prevent the binding of single or multiple effector proteins and the engagement of specific signaling pathways. The most severe mutants of this series, Fgfr1FCPG and Fgfr2FCPG, are unable to signal through FRS2, CRK, PLC and GRB14 yet fail to fully recapitulate general or conditional Fgfr1 and Fgfr2 null mutant phenotypes, indicating that additional downstream signaling pathways remain active. To identify these remaining signaling pathways, the postdoctoral fellow will conduct a proteomic screen in mouse embryonic palatal mesenchyme cells using endogenous epitope tagged FGFR1 and FGFR2 receptors, and assess the role of novel effectors in mediating FGFR1/2 activity. In a complementary approach, the postdoctoral fellow will generate mice in which additional candidate tyrosine phosphorylation sites are disrupted on the receptors, alone or in combination with the FCPG mutations. These studies will identify the signaling mechanisms driven by FGFs required for craniofacial development.