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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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Defects in epibranchial placode formation and neuronal differentiation in Sprouty mutant embryos. Whole mount in situ hybridisation with a Ngn2 RNA probe (A,B) to detect the developing placodes and a NeuroD RNA probe (C–F) to identify differentiating neuroblasts. Arrows indicate changes in gene expression and asterisks highlight regions where gene expression had been lost. Annotations are the same as in Figs. 1 and 2; with the vestibulo-acoustic nerve (VIII) also indicated. Note the enlarged geniculate placode in the Spry1−/−;Spry2−/− E9.5 embryos compared to Spry1+/−;Spry2+/− controls (A,B) (n = 6). Conversely, note the smaller or absent petrosal and nodose placodes in the Spry1−/−;Spry2−/− embryos. NeuroD expression is reduced at E9.5 (C,D) (n = 4). NeuroD expression recovers and appears increased in the geniculate (red arrow), geniculate and petrosal (green arrows) ganglia of Spry1−/−;Spry2−/− embryos compared to Spry1+/−;Spry2+/− controls (n = 4) at E10.5 (E,F).
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f0015: Defects in epibranchial placode formation and neuronal differentiation in Sprouty mutant embryos. Whole mount in situ hybridisation with a Ngn2 RNA probe (A,B) to detect the developing placodes and a NeuroD RNA probe (C–F) to identify differentiating neuroblasts. Arrows indicate changes in gene expression and asterisks highlight regions where gene expression had been lost. Annotations are the same as in Figs. 1 and 2; with the vestibulo-acoustic nerve (VIII) also indicated. Note the enlarged geniculate placode in the Spry1−/−;Spry2−/− E9.5 embryos compared to Spry1+/−;Spry2+/− controls (A,B) (n = 6). Conversely, note the smaller or absent petrosal and nodose placodes in the Spry1−/−;Spry2−/− embryos. NeuroD expression is reduced at E9.5 (C,D) (n = 4). NeuroD expression recovers and appears increased in the geniculate (red arrow), geniculate and petrosal (green arrows) ganglia of Spry1−/−;Spry2−/− embryos compared to Spry1+/−;Spry2+/− controls (n = 4) at E10.5 (E,F).

Mentions: One of the first markers for epibranchial placode specification is the proneural gene, Ngn2 (Fode et al., 1998; Sommer et al., 1996). To assess whether the specification of individual epibranchial placodes was compromised in the Sprouty mutants, whole mount in situ hybridisation using a Ngn2 riboprobe was performed at E9.5 (Fig. 3A). Ngn2 expression was expanded at the anterodorsal margin of the second arch, indicating an enlargement of the geniculate placode in the Spry1−/−;Spry2−/− embryos (Fig. 3B; n = 4). This is in line with the observation of a larger facial ganglion in Spry1−/−;Spry2−/− embryos at E10.5 (Fig. 2). By contrast, the petrosal and nodose placodes appeared smaller or missing in the Spry1−/−;Spry2−/− mutants at E9.5 (Fig. 3B; n = 4). These observations suggest that increased RTK signalling has opposite effects on the geniculate versus petrosal and nodose placodes at the time of their formation.


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

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

Defects in epibranchial placode formation and neuronal differentiation in Sprouty mutant embryos. Whole mount in situ hybridisation with a Ngn2 RNA probe (A,B) to detect the developing placodes and a NeuroD RNA probe (C–F) to identify differentiating neuroblasts. Arrows indicate changes in gene expression and asterisks highlight regions where gene expression had been lost. Annotations are the same as in Figs. 1 and 2; with the vestibulo-acoustic nerve (VIII) also indicated. Note the enlarged geniculate placode in the Spry1−/−;Spry2−/− E9.5 embryos compared to Spry1+/−;Spry2+/− controls (A,B) (n = 6). Conversely, note the smaller or absent petrosal and nodose placodes in the Spry1−/−;Spry2−/− embryos. NeuroD expression is reduced at E9.5 (C,D) (n = 4). NeuroD expression recovers and appears increased in the geniculate (red arrow), geniculate and petrosal (green arrows) ganglia of Spry1−/−;Spry2−/− embryos compared to Spry1+/−;Spry2+/− controls (n = 4) at E10.5 (E,F).
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f0015: Defects in epibranchial placode formation and neuronal differentiation in Sprouty mutant embryos. Whole mount in situ hybridisation with a Ngn2 RNA probe (A,B) to detect the developing placodes and a NeuroD RNA probe (C–F) to identify differentiating neuroblasts. Arrows indicate changes in gene expression and asterisks highlight regions where gene expression had been lost. Annotations are the same as in Figs. 1 and 2; with the vestibulo-acoustic nerve (VIII) also indicated. Note the enlarged geniculate placode in the Spry1−/−;Spry2−/− E9.5 embryos compared to Spry1+/−;Spry2+/− controls (A,B) (n = 6). Conversely, note the smaller or absent petrosal and nodose placodes in the Spry1−/−;Spry2−/− embryos. NeuroD expression is reduced at E9.5 (C,D) (n = 4). NeuroD expression recovers and appears increased in the geniculate (red arrow), geniculate and petrosal (green arrows) ganglia of Spry1−/−;Spry2−/− embryos compared to Spry1+/−;Spry2+/− controls (n = 4) at E10.5 (E,F).
Mentions: One of the first markers for epibranchial placode specification is the proneural gene, Ngn2 (Fode et al., 1998; Sommer et al., 1996). To assess whether the specification of individual epibranchial placodes was compromised in the Sprouty mutants, whole mount in situ hybridisation using a Ngn2 riboprobe was performed at E9.5 (Fig. 3A). Ngn2 expression was expanded at the anterodorsal margin of the second arch, indicating an enlargement of the geniculate placode in the Spry1−/−;Spry2−/− embryos (Fig. 3B; n = 4). This is in line with the observation of a larger facial ganglion in Spry1−/−;Spry2−/− embryos at E10.5 (Fig. 2). By contrast, the petrosal and nodose placodes appeared smaller or missing in the Spry1−/−;Spry2−/− mutants at E9.5 (Fig. 3B; n = 4). These observations suggest that increased RTK signalling has opposite effects on the geniculate versus petrosal and nodose placodes at the time of their formation.

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