A new role for the Endothelin-1/Endothelin-A receptor signaling during early neural crest specification

The neural crest is induced at the border of the neural plate in a multistep process by signals emanated from the epidermis, neural plate and mesoderm. In this work we show for the first time the existence of a neural crest maintenance step which is dependent on signals released from the mesoderm. W...

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Bibliographic Details
Published in:Developmental biology 2008-11, Vol.323 (1), p.114-129
Main Authors: Bonano, Marcela, Tríbulo, Celeste, De Calisto, Jaime, Marchant, Lorena, Sánchez, Sara S., Mayor, Roberto, Aybar, Manuel J.
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Cell migration
Ednra
Embryo, Nonmammalian - metabolism
Embryo, Nonmammalian - physiology
Embryonic Induction - genetics
Endothelin
Endothelin-1 - genetics
Endothelin-1 - metabolism
Immunohistochemistry
In Situ Hybridization
Maintenance
Models, Biological
Neural crest
Neural Crest - metabolism
Neural Crest - physiology
Receptor, Endothelin A - genetics
Receptor, Endothelin A - metabolism
Signal Transduction - genetics
Signal Transduction - physiology
Specification
Xenopus - embryology
Xenopus - genetics
Xenopus - metabolism
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Summary:The neural crest is induced at the border of the neural plate in a multistep process by signals emanated from the epidermis, neural plate and mesoderm. In this work we show for the first time the existence of a neural crest maintenance step which is dependent on signals released from the mesoderm. We identified Endothelin-1 (Edn1) and its receptor (Ednra) as key players of this signal and we show that Edn1/Ednra signaling is required for maintenance of the neural crest by a dual mechanism of cell specification and cell survival. We show that: (i) Ednra is expressed in prospective neural crest; (ii) loss-of-function experiments with antisense morpholino or with specific chemical inhibitor suppress the expression of early neural crest markers; (iii) gain-of-function experiments expand the neural crest territory; (iv) epistatic experiments show that Ednra/Edn1 is downstream of the early neural crest gene Msx1 and upstream of the late genes Sox9 and Sox10; and (v) Edn1/Ednra signaling inhibits apoptosis and controls cell specification of the neural crest. Together, our results provide insight on a new role of Edn1/Ednra cell signaling pathway during early neural crest development.
ISSN:0012-1606
1095-564X
DOI:10.1016/j.ydbio.2008.08.007