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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

Cre reporter activity (R26R stained with X-gal (blue) or green fluorescence from RosaYFP reporter, as indicated) for the cre lines used in this study are shown in the left column. Wnt1cre and Sox17iCre embryos are E9.5 and the AP2αcre embryo is E10.5. Spry2 expression as determined by in situ hybridisation on control (cre-negative) and conditional mutant E9.5 embryos, are shown in the two columns on the right. Note the loss of Spry2 expression in neural crest cells (NCC) in the Wnt1cre conditional mutant, in the endoderm (endo) in Sox17iCre conditional mutants and in the ectoderm (ecto) + NCC in AP2αcre conditional mutants.
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f0035: Cre reporter activity (R26R stained with X-gal (blue) or green fluorescence from RosaYFP reporter, as indicated) for the cre lines used in this study are shown in the left column. Wnt1cre and Sox17iCre embryos are E9.5 and the AP2αcre embryo is E10.5. Spry2 expression as determined by in situ hybridisation on control (cre-negative) and conditional mutant E9.5 embryos, are shown in the two columns on the right. Note the loss of Spry2 expression in neural crest cells (NCC) in the Wnt1cre conditional mutant, in the endoderm (endo) in Sox17iCre conditional mutants and in the ectoderm (ecto) + NCC in AP2αcre conditional mutants.

Mentions: The mouse lines used in this study were maintained on a mixed genetic background and have been described previously: β-actin-cre (Lewandoski et al., 1997), Ap2αcre (Macatee et al., 2003), Sox17i-2A-iCre (Sox17icre) (Engert et al., 2009), Wnt1cre (Danielian et al., 1998), R26R (Soriano, 1999), Spry1tm1.1Jdli (Basson et al., 2005) and Spry2tm1.1Mrt (Shim et al., 2005). Mice carrying β-actin-cre were crossed with those carrying conditional Spry1flox and Spry2flox alleles to generate Spry1−and Spry2− alleles. Embryos lacking both genes (Spry1−/−;Spry2−/−) were produced by crossing βactinCre/βactinCre;Spry1+/−;Spry2+/− males with Spry1flox/flox;Spry2flox/flox females. For rescue experiments, βactinCre2;Spry1+/−;Spry2+/−;Fgf8+/− males were crossed with Spry1flox/flox;Spry2flox/flox females using the Fgf8tm1.2Mrt allele (Meyers et al., 1998). Tissue-specific mutants were produced by crossing Cre;Spry1flox/+;Spry2flox/+ males to Spry1flox/flox;Spry2flox/flox females. Tissue specific cre recombinase activity was confirmed using the R26R (Soriano, 1999) or RosaYFP (Srinivas et al., 2001) reporter mouse lines and in situ hybridisation for Spry1 or Spry2 (Suppl. Fig. 1).


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

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

Cre reporter activity (R26R stained with X-gal (blue) or green fluorescence from RosaYFP reporter, as indicated) for the cre lines used in this study are shown in the left column. Wnt1cre and Sox17iCre embryos are E9.5 and the AP2αcre embryo is E10.5. Spry2 expression as determined by in situ hybridisation on control (cre-negative) and conditional mutant E9.5 embryos, are shown in the two columns on the right. Note the loss of Spry2 expression in neural crest cells (NCC) in the Wnt1cre conditional mutant, in the endoderm (endo) in Sox17iCre conditional mutants and in the ectoderm (ecto) + NCC in AP2αcre conditional mutants.
© Copyright Policy
Related In: Results  -  Collection

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

f0035: Cre reporter activity (R26R stained with X-gal (blue) or green fluorescence from RosaYFP reporter, as indicated) for the cre lines used in this study are shown in the left column. Wnt1cre and Sox17iCre embryos are E9.5 and the AP2αcre embryo is E10.5. Spry2 expression as determined by in situ hybridisation on control (cre-negative) and conditional mutant E9.5 embryos, are shown in the two columns on the right. Note the loss of Spry2 expression in neural crest cells (NCC) in the Wnt1cre conditional mutant, in the endoderm (endo) in Sox17iCre conditional mutants and in the ectoderm (ecto) + NCC in AP2αcre conditional mutants.
Mentions: The mouse lines used in this study were maintained on a mixed genetic background and have been described previously: β-actin-cre (Lewandoski et al., 1997), Ap2αcre (Macatee et al., 2003), Sox17i-2A-iCre (Sox17icre) (Engert et al., 2009), Wnt1cre (Danielian et al., 1998), R26R (Soriano, 1999), Spry1tm1.1Jdli (Basson et al., 2005) and Spry2tm1.1Mrt (Shim et al., 2005). Mice carrying β-actin-cre were crossed with those carrying conditional Spry1flox and Spry2flox alleles to generate Spry1−and Spry2− alleles. Embryos lacking both genes (Spry1−/−;Spry2−/−) were produced by crossing βactinCre/βactinCre;Spry1+/−;Spry2+/− males with Spry1flox/flox;Spry2flox/flox females. For rescue experiments, βactinCre2;Spry1+/−;Spry2+/−;Fgf8+/− males were crossed with Spry1flox/flox;Spry2flox/flox females using the Fgf8tm1.2Mrt allele (Meyers et al., 1998). Tissue-specific mutants were produced by crossing Cre;Spry1flox/+;Spry2flox/+ males to Spry1flox/flox;Spry2flox/flox females. Tissue specific cre recombinase activity was confirmed using the R26R (Soriano, 1999) or RosaYFP (Srinivas et al., 2001) reporter mouse lines and in situ hybridisation for Spry1 or Spry2 (Suppl. Fig. 1).

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