Role of FGF andNogginin Neural Crest Induction

AbstractA study of the moleculesnogginand fibroblast growth factor (FGF) and its receptor in the induction of the prospective neural crest inXenopus laevisembryos has been carried out, using the expression of the geneXsluas a marker for the neural crest. We show that when a truncated FGF receptor (XFD) was expressed ectopically in order to block FGF signalingXsluexpression was inhibited. The effect of XFD onXsluwas specific and could be reversed by the coinjection of the wild-type FGF receptor (FGFR). Inhibition ofXsluexpression by XFD is not a consequence of neural plate inhibition, as was shown by analyzingXsox-2 expression. When ectoderm expressing XFD was transplanted into the prospective neural fold region of embryosXsluinduction was inhibited. The neural crest can also be induced by an interaction between neural plate and epidermis. As this induction is suppressed by the presence of XFD in the neural plate and not in the epidermis, it suggests that the neural crest is induced by FGF from the epidermis. However, treatment of neural plate with FGF was not able to induceXslugexpression, showing that in addition to FGF other non-FGF factors are also required. Previously we have suggested that the ectopic ventral expression ofXsluproduced by overexpression ofnogginmRNA resulted from an interaction ofnogginwith a ventral signal. Overexpression of XFD inhibits this effect, suggesting that FGF could be one component involved in this ventral signaling. Overexpression of FGFR produced a remarkable increase in the expression ofXsluin the posterior neural folds and around the blastopore. Injections in different blastomeres of the embryo suggest that the target cells of this effect are the ventral cells. Finally, we proposed a model in which the induction of the neural crests at the border of the neural plate requires functional FGF signaling, which possibly interacts with a neural inducer such asnoggin