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Induction and maintenance of neural crest specification in Xenopus require the Edn1/Ednra cell signaling pathway
MARCELA BONANO; CELESTE TRÍBULO; JAIME DECALISTO; ROBERTO MAYOR; SARA S. SÁNCHEZ; MANUEL J. AYBAR
Los Cocos, Córdoba
Workshop; Latest Concepts in Developmental Biology, International Workshop; 2006
The neural crest is a set of pluripotent and highly migratory cells that is exclusive of vertebrates embryo. At the present, many signals have been identified to contribute to the neural crest development. Recent findings strongly suggest that Endothelin-1/ Endothelin Receptor A (Edn-1/Ednra) cell signaling pathway is critical in the migration and patterning of particular neural crest cell subpopulations in the mouse embryo. In Xenopus embryos, we have found out that Ednra mRNA is expressed in the ectoderm layer in the prospective neural crest territory from the late gastrula stage, concomitant with the moment of neural crest induction and onwards. During neurulation stages it is expressed in migratory cephalic neural crest streams, and later in branchial arches and in the otic vesicle. In order to study the function of Edn-1/Ednra pathway in neural crest development in Xenopus, we have carried out conditional gain- and loss-of-function experiments. The microinjection of Ednra mRNA, and treatment with exogenous Edn-1 peptide produced an increase in the expression of neural crest marker genes, while the injection of morpholino antisense oligonucleotides against Ednra or treatment with BQ123, an specific inhibitor of Ednra, caused a marked decrease in the expression of neural crest markers FoxD3, Snail and Slug. Both gain- and loss-of function approaches indicated that Edn-1/Ednra pathway is also involved in the migratory process and in the control of apoptosis in neural crest cells. Additionally, using an embryological/molecular approach we evaluated the participation of mesodermal tissue in the maintenance of neural crest specification. Our results showed that mesodermal tissue supports the expression of neural crest markers probably acting as a source of Edn-1 signal. Together, our results suggest that Edn1/Ednra signaling pathway is required for neural crest induction and for the maintenance of the expression of key neural crest genes.