The Snail gene family of transcription factors plays crucial roles in different morphogenetic processes during the development of vertebrate and invertebrate embryos. In previous studies of function interference for one of the family members, Slug, we showed its involvement and neural crest formation in the chick embryo. Now we have carried out a series of gain-of-function experiments in which we show that Slug overexpression in the neural tube of the chick embryo induces an increase in neural crest production. The analysis of electroporated embryos shows that Slug can induce the expression of rhoB and an increase in the number of HNK-1-positive migratory cells, indicating that it lies upstream of them in the genetic cascade of neural crest development. The increase in neural crest production after Slug overexpression was confined to the cranial region, indicating that the mechanisms of crest induction somehow differ between head and trunk.
The expression of the two vertebrate family members, Slug and Snail, is peculiar with respect to the neural crest. Slug is not expressed in the premigratory crest in the mouse, whereas it is expressed in this cell population in the chick and the opposite is true for Snail(Sefton, M., Sánchez, S. and Nieto M. A. (1998) Development125, 3111-3121). This raises the question of whether they can be functionally equivalent. To test this hypothesis both intra- and interspecies, we have performed a series of ectopic expression experiments by electroporating chick and mouse Snail in the chick embryo hindbrain. We observe that both genes elicit the same responses in the neural tube. Our results indicate that they can be functionally equivalent, although the embryos show a higher response to the endogenous gene, chick Slug.
Metamizole sodium induce neural tube defects in a chick embryo model
