Mayor R, Guerrero N, Martínez C
Faculty of Science, University of Chile, Casilla 653, Santiago, Chile.
Dev Biol. 1997 Sep 1;189(1):1-12. doi: 10.1006/dbio.1997.8634.
A study of the molecules noggin and fibroblast growth factor (FGF) and its receptor in the induction of the prospective neural crest in Xenopus laevis embryos has been carried out, using the expression of the gene Xslu as a marker for the neural crest. We show that when a truncated 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 FGF receptor (FGFR). Inhibition of Xslu expression by XFD is not a consequence of neural plate inhibition, as was shown by analyzing Xsox-2 expression. When ectoderm expressing XFD was transplanted into the prospective neural fold region of embryos Xslu induction 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 induce Xslug expression, showing that in addition to FGF other non-FGF factors are also required. Previously we have suggested that the ectopic ventral expression of Xslu produced by overexpression of noggin mRNA resulted from an interaction of noggin with 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 of Xslu in 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 as noggin.
利用基因Xslu的表达作为神经嵴的标记，对非洲爪蟾胚胎中头蛋白和成纤维细胞生长因子（FGF）及其受体在诱导预期神经嵴过程中的作用进行了研究。我们发现，当异位表达截短的FGF受体（XFD）以阻断FGF信号传导时，Xslu的表达受到抑制。XFD对Xslu的作用具有特异性，并且通过共注射野生型FGF受体（FGFR）可以逆转这种作用。通过分析Xsox-2的表达表明，XFD对Xslu表达的抑制不是神经板抑制的结果。当将表达XFD的外胚层移植到胚胎的预期神经褶区域时，Xslu的诱导受到抑制。神经嵴也可以由神经板和表皮之间的相互作用诱导产生。由于这种诱导在神经板中存在XFD时受到抑制，而在表皮中不存在XFD时不受抑制，这表明神经嵴是由来自表皮的FGF诱导产生的。然而，用FGF处理神经板并不能诱导Xslug的表达，这表明除了FGF之外，还需要其他非FGF因子。此前我们曾提出，头蛋白mRNA过表达产生的Xslu异位腹侧表达是由于头蛋白与腹侧信号相互作用的结果。XFD的过表达抑制了这种作用，这表明FGF可能是参与这种腹侧信号传导的一个成分。FGFR的过表达导致后神经褶和胚孔周围Xslu的表达显著增加。在胚胎的不同卵裂球中注射表明，这种作用的靶细胞是腹侧细胞。最后，我们提出了一个模型，其中神经板边界处神经嵴的诱导需要功能性的FGF信号传导，该信号传导可能与诸如头蛋白的神经诱导剂相互作用。
