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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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Cranial nerve abnormalities in Sprouty mutants. Anti-neurofilament immunohistochemistry revealing developing cranial nerves of wildtype (A), Spry1−/− (B), Spry2−/− (C), Spry1+/−;Spry2+/− (D) and Spry1−/−;Spry2−/− (E,E′) E10.5 embryos is shown. All embryos were between 34 and 36 somite stage. Standard labelling of the cranial nerves was used, trigeminal ganglion (V) with opthalmic (Vo), maxillary (Vmx) and mandibulary (Vm) branches, facial nerve (VII); vestibulocochlear nerve (VIII); glossopharyngeal nerve (IX) and the vagus nerve (X). Arrows highlight abnormal morphology and asterisks indicate missing portions. The majority of developing cranial nerves present in Spry1−/− (B), Spry2−/− (C) and Spry1+/−;Spry2+/− (D) embryos were comparable to wildtype and the latter genotype was used as a control in this study. Spry1−/−;Spry2−/− embryos have trigeminal defects (e.g. absent ophthalmic branch of the trigeminal nerve in E), facial nerve defects and glossopharyngeal and vagus cranial nerves display incomplete or irregular bridging between proximal and distal ganglia (E,E′). (F–M) Neurofilament (RMO-270) and Phox2b immunohistochemistry counter stained with DAPI on sections from E10.5 Spry1+/−;Spry2+/− control (F–I) and Spry1−/−;Spry2−/− (J–M) mutant embryos. Neurofilament staining is indicated with green fluorescence, Phox2b labelling of motor and sensory neuron nuclei in red and DAPI stained nuclei in blue. Labelling of markers and genotypes of merged images are as indicated. Other labels include, facial cranial nerve (VII) with motor nuclei in rhombomere 4 of the hindbrain (VIIm) and sensory neuron nuclei in the developing geniculate ganglion (VIIg). The white lines in F and J indicate plane of section for the images on the right. Motor nuclei are present in rhombomere 4 of the hindbrain in both the Spry1−/−;Spry2−/− mutant and Spry1+/−;Spry2+/− control embryos and are positioned adjacent to the developing geniculate ganglion (n = 4). The geniculate ganglion is enlarged in the Spry1−/−;Spry2−/− embryos compared to the Spry1+/−;Spry2+/− controls (compare white arrows in G with K).
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f0010: Cranial nerve abnormalities in Sprouty mutants. Anti-neurofilament immunohistochemistry revealing developing cranial nerves of wildtype (A), Spry1−/− (B), Spry2−/− (C), Spry1+/−;Spry2+/− (D) and Spry1−/−;Spry2−/− (E,E′) E10.5 embryos is shown. All embryos were between 34 and 36 somite stage. Standard labelling of the cranial nerves was used, trigeminal ganglion (V) with opthalmic (Vo), maxillary (Vmx) and mandibulary (Vm) branches, facial nerve (VII); vestibulocochlear nerve (VIII); glossopharyngeal nerve (IX) and the vagus nerve (X). Arrows highlight abnormal morphology and asterisks indicate missing portions. The majority of developing cranial nerves present in Spry1−/− (B), Spry2−/− (C) and Spry1+/−;Spry2+/− (D) embryos were comparable to wildtype and the latter genotype was used as a control in this study. Spry1−/−;Spry2−/− embryos have trigeminal defects (e.g. absent ophthalmic branch of the trigeminal nerve in E), facial nerve defects and glossopharyngeal and vagus cranial nerves display incomplete or irregular bridging between proximal and distal ganglia (E,E′). (F–M) Neurofilament (RMO-270) and Phox2b immunohistochemistry counter stained with DAPI on sections from E10.5 Spry1+/−;Spry2+/− control (F–I) and Spry1−/−;Spry2−/− (J–M) mutant embryos. Neurofilament staining is indicated with green fluorescence, Phox2b labelling of motor and sensory neuron nuclei in red and DAPI stained nuclei in blue. Labelling of markers and genotypes of merged images are as indicated. Other labels include, facial cranial nerve (VII) with motor nuclei in rhombomere 4 of the hindbrain (VIIm) and sensory neuron nuclei in the developing geniculate ganglion (VIIg). The white lines in F and J indicate plane of section for the images on the right. Motor nuclei are present in rhombomere 4 of the hindbrain in both the Spry1−/−;Spry2−/− mutant and Spry1+/−;Spry2+/− control embryos and are positioned adjacent to the developing geniculate ganglion (n = 4). The geniculate ganglion is enlarged in the Spry1−/−;Spry2−/− embryos compared to the Spry1+/−;Spry2+/− controls (compare white arrows in G with K).

Mentions: Whole E10.5 embryos were stained with an antibody to neurofilament to reveal the developing cranial nerves (Figs. 2A–E′). Cranial nerves in Spry1−/− (n = 9/10) and Spry2−/− (n = 8/8) embryos exhibited normal morphologies when compared to wildtype controls (n = 10) at E10.5 (compare Figs. 2B and C with A, Table 1). Most Spry+/−;Spry2+/− embryos (n = 28/34) also exhibited no cranial nerve defects, confirming that the loss of two Sprouty alleles is insufficient to cause significant cranial nerve defects (Fig. 2D). These observations suggest that Spry1 and Spry2 may functionally compensate for the loss of each other during branchial nerve development.


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

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

Cranial nerve abnormalities in Sprouty mutants. Anti-neurofilament immunohistochemistry revealing developing cranial nerves of wildtype (A), Spry1−/− (B), Spry2−/− (C), Spry1+/−;Spry2+/− (D) and Spry1−/−;Spry2−/− (E,E′) E10.5 embryos is shown. All embryos were between 34 and 36 somite stage. Standard labelling of the cranial nerves was used, trigeminal ganglion (V) with opthalmic (Vo), maxillary (Vmx) and mandibulary (Vm) branches, facial nerve (VII); vestibulocochlear nerve (VIII); glossopharyngeal nerve (IX) and the vagus nerve (X). Arrows highlight abnormal morphology and asterisks indicate missing portions. The majority of developing cranial nerves present in Spry1−/− (B), Spry2−/− (C) and Spry1+/−;Spry2+/− (D) embryos were comparable to wildtype and the latter genotype was used as a control in this study. Spry1−/−;Spry2−/− embryos have trigeminal defects (e.g. absent ophthalmic branch of the trigeminal nerve in E), facial nerve defects and glossopharyngeal and vagus cranial nerves display incomplete or irregular bridging between proximal and distal ganglia (E,E′). (F–M) Neurofilament (RMO-270) and Phox2b immunohistochemistry counter stained with DAPI on sections from E10.5 Spry1+/−;Spry2+/− control (F–I) and Spry1−/−;Spry2−/− (J–M) mutant embryos. Neurofilament staining is indicated with green fluorescence, Phox2b labelling of motor and sensory neuron nuclei in red and DAPI stained nuclei in blue. Labelling of markers and genotypes of merged images are as indicated. Other labels include, facial cranial nerve (VII) with motor nuclei in rhombomere 4 of the hindbrain (VIIm) and sensory neuron nuclei in the developing geniculate ganglion (VIIg). The white lines in F and J indicate plane of section for the images on the right. Motor nuclei are present in rhombomere 4 of the hindbrain in both the Spry1−/−;Spry2−/− mutant and Spry1+/−;Spry2+/− control embryos and are positioned adjacent to the developing geniculate ganglion (n = 4). The geniculate ganglion is enlarged in the Spry1−/−;Spry2−/− embryos compared to the Spry1+/−;Spry2+/− controls (compare white arrows in G with K).
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f0010: Cranial nerve abnormalities in Sprouty mutants. Anti-neurofilament immunohistochemistry revealing developing cranial nerves of wildtype (A), Spry1−/− (B), Spry2−/− (C), Spry1+/−;Spry2+/− (D) and Spry1−/−;Spry2−/− (E,E′) E10.5 embryos is shown. All embryos were between 34 and 36 somite stage. Standard labelling of the cranial nerves was used, trigeminal ganglion (V) with opthalmic (Vo), maxillary (Vmx) and mandibulary (Vm) branches, facial nerve (VII); vestibulocochlear nerve (VIII); glossopharyngeal nerve (IX) and the vagus nerve (X). Arrows highlight abnormal morphology and asterisks indicate missing portions. The majority of developing cranial nerves present in Spry1−/− (B), Spry2−/− (C) and Spry1+/−;Spry2+/− (D) embryos were comparable to wildtype and the latter genotype was used as a control in this study. Spry1−/−;Spry2−/− embryos have trigeminal defects (e.g. absent ophthalmic branch of the trigeminal nerve in E), facial nerve defects and glossopharyngeal and vagus cranial nerves display incomplete or irregular bridging between proximal and distal ganglia (E,E′). (F–M) Neurofilament (RMO-270) and Phox2b immunohistochemistry counter stained with DAPI on sections from E10.5 Spry1+/−;Spry2+/− control (F–I) and Spry1−/−;Spry2−/− (J–M) mutant embryos. Neurofilament staining is indicated with green fluorescence, Phox2b labelling of motor and sensory neuron nuclei in red and DAPI stained nuclei in blue. Labelling of markers and genotypes of merged images are as indicated. Other labels include, facial cranial nerve (VII) with motor nuclei in rhombomere 4 of the hindbrain (VIIm) and sensory neuron nuclei in the developing geniculate ganglion (VIIg). The white lines in F and J indicate plane of section for the images on the right. Motor nuclei are present in rhombomere 4 of the hindbrain in both the Spry1−/−;Spry2−/− mutant and Spry1+/−;Spry2+/− control embryos and are positioned adjacent to the developing geniculate ganglion (n = 4). The geniculate ganglion is enlarged in the Spry1−/−;Spry2−/− embryos compared to the Spry1+/−;Spry2+/− controls (compare white arrows in G with K).
Mentions: Whole E10.5 embryos were stained with an antibody to neurofilament to reveal the developing cranial nerves (Figs. 2A–E′). Cranial nerves in Spry1−/− (n = 9/10) and Spry2−/− (n = 8/8) embryos exhibited normal morphologies when compared to wildtype controls (n = 10) at E10.5 (compare Figs. 2B and C with A, Table 1). Most Spry+/−;Spry2+/− embryos (n = 28/34) also exhibited no cranial nerve defects, confirming that the loss of two Sprouty alleles is insufficient to cause significant cranial nerve defects (Fig. 2D). These observations suggest that Spry1 and Spry2 may functionally compensate for the loss of each other during branchial nerve development.

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