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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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Related in: MedlinePlus

Neural crest cell fate appears altered in Spry1−/−;Spry2−/− embryos. Whole mount in situ hybridisation of control (A,C,E,G) and Spry1−/−;Spry2−/− embryos (B,D,F,H) with neural crest markers Crabp1 (A,B) (n = 6), Sox10 (C,D) (n = 4), Dlx2 (E,F) (n = 4), and a reporter of FGF signalling Erm (G,H) all at E9 (20–22 somite stage). Neural crest streams, pharyngeal arches and otic vesicle are labelled as in Figs. 1 and 2. Arrows illustrate changes in gene expression and asterisks indicate regions with absent gene expression.
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f0020: Neural crest cell fate appears altered in Spry1−/−;Spry2−/− embryos. Whole mount in situ hybridisation of control (A,C,E,G) and Spry1−/−;Spry2−/− embryos (B,D,F,H) with neural crest markers Crabp1 (A,B) (n = 6), Sox10 (C,D) (n = 4), Dlx2 (E,F) (n = 4), and a reporter of FGF signalling Erm (G,H) all at E9 (20–22 somite stage). Neural crest streams, pharyngeal arches and otic vesicle are labelled as in Figs. 1 and 2. Arrows illustrate changes in gene expression and asterisks indicate regions with absent gene expression.

Mentions: Whole-mount in situ hybridisation for a pan-neural crest marker Crabp1 showed that all the neural crest streams were present and migrating to the appropriate regions in the Spry1−/−;Spry2−/− mutants (Figs. 4A,B; n = 8). To distinguish between ectomesenchymal and non-ectomesechymal neural crest cells we used Dlx2 and Sox10 as respective markers (Baker et al., 1997; Blentic et al., 2008). The intensity of Sox10 expression where the hyoid neural crest stream approaches the geniculate placode was slightly reduced in Spry1−/−;Spry2−/− mutants (red arrow, Figs. 4C,D; n = 8). Intriguingly, Dlx2 expression appeared to respond in the opposite manner and was markedly upregulated in this region (red arrows, Figs. 4E,F; n = 4). These gene expression changes are consistent with a change in neural crest cell fate from non-ectomesenchymal to ectomesenchymal in the vicinity of the geniculate placode. Sox10 expression was also decreased in the post otic stream where the petrosal and nodose placodes develop (green asterisks, Figs. 4C,D; n = 8), although no corresponding up-regulation of Dlx2 expression in the third and developing fourth pharyngeal arches was observed (Figs. 4E,F; n = 4).


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

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

Neural crest cell fate appears altered in Spry1−/−;Spry2−/− embryos. Whole mount in situ hybridisation of control (A,C,E,G) and Spry1−/−;Spry2−/− embryos (B,D,F,H) with neural crest markers Crabp1 (A,B) (n = 6), Sox10 (C,D) (n = 4), Dlx2 (E,F) (n = 4), and a reporter of FGF signalling Erm (G,H) all at E9 (20–22 somite stage). Neural crest streams, pharyngeal arches and otic vesicle are labelled as in Figs. 1 and 2. Arrows illustrate changes in gene expression and asterisks indicate regions with absent gene expression.
© Copyright Policy
Related In: Results  -  Collection

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

f0020: Neural crest cell fate appears altered in Spry1−/−;Spry2−/− embryos. Whole mount in situ hybridisation of control (A,C,E,G) and Spry1−/−;Spry2−/− embryos (B,D,F,H) with neural crest markers Crabp1 (A,B) (n = 6), Sox10 (C,D) (n = 4), Dlx2 (E,F) (n = 4), and a reporter of FGF signalling Erm (G,H) all at E9 (20–22 somite stage). Neural crest streams, pharyngeal arches and otic vesicle are labelled as in Figs. 1 and 2. Arrows illustrate changes in gene expression and asterisks indicate regions with absent gene expression.
Mentions: Whole-mount in situ hybridisation for a pan-neural crest marker Crabp1 showed that all the neural crest streams were present and migrating to the appropriate regions in the Spry1−/−;Spry2−/− mutants (Figs. 4A,B; n = 8). To distinguish between ectomesenchymal and non-ectomesechymal neural crest cells we used Dlx2 and Sox10 as respective markers (Baker et al., 1997; Blentic et al., 2008). The intensity of Sox10 expression where the hyoid neural crest stream approaches the geniculate placode was slightly reduced in Spry1−/−;Spry2−/− mutants (red arrow, Figs. 4C,D; n = 8). Intriguingly, Dlx2 expression appeared to respond in the opposite manner and was markedly upregulated in this region (red arrows, Figs. 4E,F; n = 4). These gene expression changes are consistent with a change in neural crest cell fate from non-ectomesenchymal to ectomesenchymal in the vicinity of the geniculate placode. Sox10 expression was also decreased in the post otic stream where the petrosal and nodose placodes develop (green asterisks, Figs. 4C,D; n = 8), although no corresponding up-regulation of Dlx2 expression in the third and developing fourth pharyngeal arches was observed (Figs. 4E,F; n = 4).

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