Imaging the cellular behaviors and interactions governing zebrafish palatogenesis

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As in amniotes, zebrafish neural crest cells that migrate around the eye to condense upon the oral ectoderm form the palate. We have found that Pdgf signaling mediates crest cell migration and that Shh signaling regulates crest condensation. Mutation of pdgf receptor a (pdgfra) causes cleft palate and loss of oral ectodermal gene expression. Time‐lapse microscopy demonstrates that crest cells fail to migrate to the oral ectoderm in pdgfra mutants. Genetic mosaics show that crest require reception of Pdgf signaling for proper migration. Additionally, loss of oral ectodermal gene expression in pdgfra mutants is a secondary defect caused by the absence of crest, demonstrating that crest‐derived signals induce oral ectodermal gene expression. Mutation of the Shh receptor smoothened causes failure of crest condensation and loss of oral ectodermal gene expression. Genetic mosaics show that wild‐type oral ectoderm transplanted into smoothened mutants rescues crest condensation, demonstrating crest cells require signals from the oral ectoderm to condense. Cyclopamine treatment demonstrates that the oral ectoderm requires Shh signaling at the end of gastrulation, prior to crest cell migration. Collectively, these results suggest a model where Shh establishes competence of the oral ectoderm to respond to crest‐derived signals, following Pdgf mediated cell migration to the oral ectoderm.