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Sprouty genes are essential for the normal development of epibranchial ganglia in the mouse embryo.

Simrick S, Lickert H, Basson MA - Dev. Biol. (2011)

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.

View Article: PubMed Central - PubMed

Affiliation: Department of Craniofacial Development, King's College London, Floor 27, Guy's Tower, London, SE1 9RT, UK.

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Sprouty function in the pharyngeal epithelia is required for normal facial nerve morphogenesis. (A–D) Anti-neurofilament (RMO-270) whole mount immunohistochemistry revealing cranial nerve morphology in Spry1 and Spry2 tissue specific conditional knockout E10.5 embryos. Tissue specific gene deletion was achieved using the cre-lox system with Spry1 and Spry2 flox alleles and Wnt1cre (B, neural crest), Ap2αcre (C, ectoderm and neural crest), and Sox17icre (D, endoderm). A stage-matched Spry1f/+;Spry2f/+ litter-mate control is displayed to indicate normal cranial nerve morphology (A). Genotypes are as indicated and labels are as before. Red arrows illustrate changes in cranial nerve morphology. (E–J) Whole mount in situ hybridisation with Ngn2 antisense RNA probe to reveal the epibranchial placodes in Wnt1cre-, AP2acre-, or Sox17icre-mediated conditional knockout (cko) embryos as indicated. Note the enlarged geniculate placode and slightly smaller petrosal in the Ap2αcre;Spry1f/−;Spry2f/−and Sox17cre;Spry1f/f;Spry2f/f embryos (red arrows in H and J). The epibranchial placodes, geniculate (G), petrosal (P) and nodose (N) are labelled.
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f0025: Sprouty function in the pharyngeal epithelia is required for normal facial nerve morphogenesis. (A–D) Anti-neurofilament (RMO-270) whole mount immunohistochemistry revealing cranial nerve morphology in Spry1 and Spry2 tissue specific conditional knockout E10.5 embryos. Tissue specific gene deletion was achieved using the cre-lox system with Spry1 and Spry2 flox alleles and Wnt1cre (B, neural crest), Ap2αcre (C, ectoderm and neural crest), and Sox17icre (D, endoderm). A stage-matched Spry1f/+;Spry2f/+ litter-mate control is displayed to indicate normal cranial nerve morphology (A). Genotypes are as indicated and labels are as before. Red arrows illustrate changes in cranial nerve morphology. (E–J) Whole mount in situ hybridisation with Ngn2 antisense RNA probe to reveal the epibranchial placodes in Wnt1cre-, AP2acre-, or Sox17icre-mediated conditional knockout (cko) embryos as indicated. Note the enlarged geniculate placode and slightly smaller petrosal in the Ap2αcre;Spry1f/−;Spry2f/−and Sox17cre;Spry1f/f;Spry2f/f embryos (red arrows in H and J). The epibranchial placodes, geniculate (G), petrosal (P) and nodose (N) are labelled.

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.


Sprouty genes are essential for the normal development of epibranchial ganglia in the mouse embryo.

Simrick S, Lickert H, Basson MA - Dev. Biol. (2011)

Sprouty function in the pharyngeal epithelia is required for normal facial nerve morphogenesis. (A–D) Anti-neurofilament (RMO-270) whole mount immunohistochemistry revealing cranial nerve morphology in Spry1 and Spry2 tissue specific conditional knockout E10.5 embryos. Tissue specific gene deletion was achieved using the cre-lox system with Spry1 and Spry2 flox alleles and Wnt1cre (B, neural crest), Ap2αcre (C, ectoderm and neural crest), and Sox17icre (D, endoderm). A stage-matched Spry1f/+;Spry2f/+ litter-mate control is displayed to indicate normal cranial nerve morphology (A). Genotypes are as indicated and labels are as before. Red arrows illustrate changes in cranial nerve morphology. (E–J) Whole mount in situ hybridisation with Ngn2 antisense RNA probe to reveal the epibranchial placodes in Wnt1cre-, AP2acre-, or Sox17icre-mediated conditional knockout (cko) embryos as indicated. Note the enlarged geniculate placode and slightly smaller petrosal in the Ap2αcre;Spry1f/−;Spry2f/−and Sox17cre;Spry1f/f;Spry2f/f embryos (red arrows in H and J). The epibranchial placodes, geniculate (G), petrosal (P) and nodose (N) are labelled.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC3368431&req=5

f0025: Sprouty function in the pharyngeal epithelia is required for normal facial nerve morphogenesis. (A–D) Anti-neurofilament (RMO-270) whole mount immunohistochemistry revealing cranial nerve morphology in Spry1 and Spry2 tissue specific conditional knockout E10.5 embryos. Tissue specific gene deletion was achieved using the cre-lox system with Spry1 and Spry2 flox alleles and Wnt1cre (B, neural crest), Ap2αcre (C, ectoderm and neural crest), and Sox17icre (D, endoderm). A stage-matched Spry1f/+;Spry2f/+ litter-mate control is displayed to indicate normal cranial nerve morphology (A). Genotypes are as indicated and labels are as before. Red arrows illustrate changes in cranial nerve morphology. (E–J) Whole mount in situ hybridisation with Ngn2 antisense RNA probe to reveal the epibranchial placodes in Wnt1cre-, AP2acre-, or Sox17icre-mediated conditional knockout (cko) embryos as indicated. Note the enlarged geniculate placode and slightly smaller petrosal in the Ap2αcre;Spry1f/−;Spry2f/−and Sox17cre;Spry1f/f;Spry2f/f embryos (red arrows in H and J). The epibranchial placodes, geniculate (G), petrosal (P) and nodose (N) are labelled.
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.

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.

View Article: PubMed Central - PubMed

Affiliation: Department of Craniofacial Development, King's College London, Floor 27, Guy's Tower, London, SE1 9RT, UK.

Show MeSH
Related in: MedlinePlus