Multiple Cranial Organ Defects after Conditionally Knocking OutFgf10in the Neural Crest.
Fgf10is necessary for the development of a number of organs that fail to develop or are reduced in size in the null mutant. Here we have knocked outFgf10specifically in the neural crest driven byWnt1cre. TheWnt1creFgf10fl/flmouse phenocopies many of the null mutant defects, including cleft palate, loss of salivary glands, and ocular glands, highlighting the neural crest origin of theFgf10expressing mesenchyme surrounding these organs. In contrast tissues such as the limbs and lungs, whereFgf10is expressed by the surrounding mesoderm, were unaffected, as was the pituitary gland whereFgf10is expressed by the neuroepithelium. The circumvallate papilla of the tongue formed but was hypoplastic in the conditional andFgf10null embryos, suggesting that other sources of FGF can compensate in development of this structure. The tracheal cartilage rings showed normal patterning in the conditional knockout, indicating that the source ofFgf10for this tissue is mesodermal, which was confirmed usingWnt1cre-dtTomto lineage trace the boundary of the neural crest in this region. The thyroid, thymus, and parathyroid glands surrounding the trachea were present but hypoplastic in the conditional mutant, indicating that a neighboring source of mesodermalFgf10might be able to partially compensate for loss of neural crest derivedFgf10.
Department of Stomatology, School of Dentistry, University of Sao Paulo São Paulo, Brazil.
Tathyane H N
TH
Teshima
Department of Stomatology, School of Dentistry, University of Sao Paulo São Paulo, Brazil.
Silvia V
SV
Lourenco
Department of Craniofacial Development and Stem Cell Biology, King's College London London, UK.
Abigail S
AS
Tucker
CVP; Fgf10; cranial glands; ocular glands; palate; thyroid