Wnt6 controls amniote neural crest induction through the non‐canonical signaling pathway

The neural crest is a multipotent embryonic cell population that arises from neural ectoderm and forms derivatives essential for vertebrate function. Neural crest induction requires an ectodermal signal, thought to be a Wnt ligand, but the identity of the Wnt that performs this function in amniotes...

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Bibliographic Details
Published in:Developmental dynamics 2007-09, Vol.236 (9), p.2502-2511
Main Authors: Schmidt, Corina, McGonnell, Imelda M., Allen, Steve, Otto, Anthony, Patel, Ketan
Format: Article
Language:English
Subjects:
Acetylcysteine - metabolism
Amnion - physiology
Animals
Cells, Cultured
Chick Embryo
Developmental Biology - methods
Electroporation
Gene Expression Regulation, Developmental
induction
Ligands
Mice
Models, Biological
neural crest
Neural Crest - embryology
Neural Crest - metabolism
NIH 3T3 Cells
non‐canonical
Signal Transduction
Wnt Proteins - genetics
Wnt Proteins - physiology
Wnt1
Wnt6
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Summary:The neural crest is a multipotent embryonic cell population that arises from neural ectoderm and forms derivatives essential for vertebrate function. Neural crest induction requires an ectodermal signal, thought to be a Wnt ligand, but the identity of the Wnt that performs this function in amniotes is unknown. Here, we demonstrate that Wnt6, derived from the ectoderm, is necessary for chick neural crest induction. Crucially, we also show that Wnt6 acts through the non‐canonical pathway and not the beta‐catenin–dependant pathway. Surprisingly, we found that canonical Wnt signaling inhibited neural crest production in the chick embryo. In light of studies in anamniotes demonstrating that canonical Wnt signaling induces neural crest, these results indicate a significant and novel change in the mechanism of neural crest induction during vertebrate evolution. These data also highlight a key role for noncanonical Wnt signaling in cell type specification from a stem population during development. Developmental Dynamics 236:2502–2511, 2007. © 2007 Wiley‐Liss, Inc.
ISSN:1058-8388
1097-0177
DOI:10.1002/dvdy.21260