Sprouty genes are essential for the normal development of epibranchial ganglia in the mouse embryo.
Bottom Line: Fibroblast growth factor (FGF) signalling has important roles in the development of the embryonic pharyngeal (branchial) arches, but its effects on innervation of the arches and associated structures have not been studied extensively.However, epithelial-specific gene deletion only results in defects in the facial nerve and not the glossopharyngeal and vagus nerves, suggesting that the facial nerve is most sensitive to perturbations in RTK signalling.Reducing the Fgf8 gene dosage only partially rescued defects in the glossopharyngeal nerve and was not sufficient to rescue facial nerve defects, suggesting that FGF8 is functionally redundant with other RTK ligands during facial nerve development.
Affiliation: Department of Craniofacial Development, King's College London, Floor 27, Guy's Tower, London, SE1 9RT, UK.Show MeSH
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Mentions: We next asked whether the defects in neural crest and placodal development were cell autonomous in Spry1−/−;Spry2−/− mutants. Spry1 and Spry2 were excised in different tissues using several cre lines. No defects were detected in E10.5 Wnt1cre;Spry1f/−;Spry2f/−embryos (n = 8), indicating that the loss of Sprouty genes in the neural crest is not sufficient to cause cranial nerve defects (Figs. 5A,B, Table 1). Furthermore Ngn2 expression was normal in the epibranchial placodes of these mutants (Figs. 5E,F; n = 4), indicating that defects in the development of the epibranchial placodes were not caused by defects in the neural crest alone.
Affiliation: Department of Craniofacial Development, King's College London, Floor 27, Guy's Tower, London, SE1 9RT, UK.