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Wnt6 controls amniote neural crest induction through the non‐canonical signaling pathway
Author(s) -
Schmidt Corina,
McGonnell Imelda M.,
Allen Steve,
Otto Anthony,
Patel Ketan
Publication year - 2007
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.21260
Subject(s) - neural crest , biology , ectoderm , wnt signaling pathway , amniote , population , microbiology and biotechnology , neural fold , beta catenin , neural plate , vertebrate , anatomy , neuroscience , genetics , embryogenesis , signal transduction , embryo , gene , demography , sociology
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.