We have used the maternal effect mutant ichabod, which is deficient in maternal beta-catenin signaling, to test for the epistatic relationship between beta-catenin activation, FGF signaling and bozozok, squint and chordin expression. Injection of beta-catenin RNA into ichabod embryos can completely rescue normal development. By contrast, when FGF signaling is inhibited, beta-catenin did not induce goosecoid and chordin, repress bmp4 expression or induce a dorsal axis. These results demonstrate that FGF signaling is necessary for beta-catenin induction of the zebrafish organizer. We show that FGFs function downstream of squint and bozozok to turn on chordin expression. Full rescue of ichabod by Squint is dependent on FGF signaling, and partial rescue by FGFs is completely dependent on chordin. By contrast, Bozozok can rescue the complete anteroposterior axis, but not notochord, in embryos blocked in FGF signaling. Surprisingly, accumulation of bozozok transcript in beta-catenin RNA-injected ichabod embryos is also dependent on FGF signaling, indicating a role of FGFs in maintenance of bozozok RNA. These experiments show that FGF-dependent organizer function operates through both bozozok RNA accumulation and a pathway consisting of beta-catenin-->Squint-->FGF-->Chordin, in which each component is sufficient for expression of the downstream factors of the pathway, and in which Nodal signaling is required for FGF gene expression and FGF signaling is required for Squint induction of chordin.