ROLE OF FGF AND NOGGIN IN NEURAL CREST INDUCTION

A study of the molecules noggin and fibroblast growth factor (FGF) and its receptor in the induction of the prospective neural crest in Xeno pus laevis embryos has been carried out, using the expression of the g ene Xslu as a marker for the neural crest. We show that when a truncat ed FGF receptor (XFD) was expressed ectopically in order to block FGF signaling Xslu expression was inhibited. The effect of XFD on Xslu was specific and could be reversed by the coinjection of the wild-type FG F receptor (FGFR). Inhibition of Xslu expression by XFD is not a conse quence of neural plate inhibition, as was shown by analyzing Xsox-2 ex pression. When ectoderm expressing XFD was transplanted into the prosp ective neural fold region of embryos Xslu induction was inhibited. The neural crest can also be induced by an interaction between neural pla te and epidermis. As this induction is suppressed by the presence of X FD 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 induce Xslug expression, show ing that in addition to FGF other non-FGF factors are also required. P reviously we have suggested that the ectopic ventral expression of Xsl u produced by overexpression of noggin mRNA resulted from an interacti on of noggin with a ventral signal. Overexpression of XFD inhibits thi s effect, suggesting that FGF could be one component involved in this ventral signaling. Overexpression of FGFR produced a remarkable increa se in the expression of Xslu in the posterior neural folds and around the blastopore. Injections in different blastomeres of the embryo sugg est that the target cells of this effect are the ventral cells. Finall y, we proposed a model in which the induction of the neural crests at the border of the neural plate requires functional FGF signaling, whic h possibly interacts with a neural inducer such as noggin. (C) 1997 Ac ademic Press.