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An early role for sonic hedgehog from foregut endoderm in jaw development: ensuring neural crest cell survival
José M Brito1, Marie-Aimée Teillet, Nicole M Le Douarin
1Laboratoire de Développement, Evolution et Plasticité du Système Nerveux, Unité Propre de Recherche 2197, Centre National de la Recherche Scientifique, Institut de Neurobiologie Alfred Fessard, F-91198 Gif-sur-Yvette, France.
Insights
Sonic hedgehog (Shh) from the ventral foregut endoderm is crucial for lower jaw development. Supplying exogenous Shh rescued facial structure defects in chicken embryos, confirming its role in neural crest cell survival.
Area of Science:
- Developmental biology
- Embryology
- Molecular biology
Background:
- Sonic hedgehog (Shh) is a key signaling molecule in embryonic development.
- Facial structure formation is a complex process involving multiple signaling pathways.
- Neural crest cells (NCCs) are vital for craniofacial development.
Purpose of the Study:
- To investigate the role of Sonic hedgehog (Shh) in chicken embryo facial development.
- To determine the impact of Shh deprivation on neural crest cell survival and branchial arch development.
- To elucidate the source and function of Shh in lower jaw formation.
Main Methods:
- Surgical removal of anterior embryonic tissues (forehead, prechordal plate, ventral foregut endoderm) at specific developmental stages (5-10 somite stages).
- Observation of facial structure development, including lower jaw formation.
- Analysis of neural crest cell migration and apoptosis in the first branchial arch (BA1).
- Administration of exogenous Shh to operated embryos.
Main Results:
- Forehead removal before 7 somite stages resulted in lower jaw absence, while later removal (8-10 somite stages) led to lower beak formation.
- Early Shh deprivation caused massive NCC apoptosis in BA1.
- Exogenous Shh administration rescued lower jaw development in early-operated embryos.
- Shh expression in the ventral foregut endoderm was linked to NCC survival and BA1 development.
Conclusions:
- Sonic hedgehog (Shh) signaling from the ventral foregut endoderm is essential for the survival of neural crest cells during early first branchial arch development.
- Shh plays a critical role in regulating lower jaw formation in chicken embryos.
- The timing of Shh signaling is crucial for preventing NCC apoptosis and ensuring proper craniofacial morphogenesis.
Abstract:
We have investigated the role of Sonic hedgehog (Shh) in the development of facial structures by depriving chicken embryos of the most anterior sources of this morphogen, including the prechordal plate and the anterior ventral endoderm of the foregut, before the onset of neural crest cell (NCC) migration to the first branchial arch (BA1). The entire forehead, including the foregut endoderm, was removed at 5- to 10-somite stage (ss), which led to the absence of the lower jaw when the operation was performed before 7-ss. If the embryos were deprived of their forehead at 8- to 10-ss, they were later on endowed with a lower beak. In embryos that were operated on early, the NCCs migrated normally to BA1 but were subjected to massive apoptosis a few hours later. Cell death did not occur when forehead excision was performed at a later stage. In this case, onward expression of Shh in the ventral foregut endoderm extended caudally over the excision limit, and we hypothesized that absence of Shh production by the endoderm in embryos that were operated on early could be responsible for the NCC apoptosis and the failure of BA1 development. We thus provided exogenous Shh to the embryos that were operated on before 7-ss. In this case, the development of the lower jaw was rescued. Therefore, Shh derived from the ventral foregut endoderm ensures the survival of NCCs at a critical stage of BA1 development.
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