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.