Pharyngeal Ectoderm Research Articles

Fgfr1regulates patterning of the pharyngeal region

Development of the pharyngeal region depends on the interaction and integration of different cell populations, including surface ectoderm, foregut endoderm, paraxial mesoderm, and neural crest. Mice homozygous for a hypomorphic allele of Fgfr1 have craniofacial defects, some of which appeared to result from a failure in the early development of the second branchial arch. A stream of neural crest cells was found to originate from the rhombomere 4 region and migrate toward the second branchial arch in the mutants. Neural crest cells mostly failed to enter the second arch, however, but accumulated in a region proximal to it. Both rescue of the hypomorphic Fgfr1 allele and inactivation of a conditional Fgfr1 allele specifically in neural crest cells indicated that Fgfr1 regulates the entry of neural crest cells into the second branchial arch non-cell-autonomously. Gene expression in the pharyngeal ectoderm overlying the developing second branchial arch was affected in the hypomorphic Fgfr1 mutants at a stage prior to neural crest entry. Our results indicate that Fgfr1 patterns the pharyngeal region to create a permissive environment for neural crest cell migration.

Fgf8is required for pharyngeal arch and cardiovascular development in the mouse

We present here an analysis of cardiovascular and pharyngeal arch development in mouse embryos hypomorphic for Fgf8. Previously, we have described the generation of Fgf8 compound heterozygous (Fgf8(neo/-)) embryos. Although early analysis demonstrated that some of these embryos have abnormal left-right (LR) axis specification and cardiac looping reversals, the number and type of cardiac defects present at term suggested an additional role for Fgf8 in cardiovascular development. Most Fgf8(neo/-) mutant embryos survive to term with abnormal cardiovascular patterning, including outflow tract, arch artery and intracardiac defects. In addition, these mutants have hypoplastic pharyngeal arches, small or absent thymus and abnormal craniofacial development. Neural crest cells (NCCs) populate the pharyngeal arches and contribute to many structures of the face, neck and cardiovascular system, suggesting that Fgf8 may be required for NCC development. Fgf8 is expressed within the developing pharyngeal arch ectoderm and endoderm during NCC migration through the arches. Analysis of NCC development in Fgf8(neo/-) mutant embryos demonstrates that NCCs are specified and migrate, but undergo cell death in areas both adjacent and distal to where Fgf8 is normally expressed. This study defines the cardiovascular defects present in Fgf8 mutants and supports a role for Fgf8 in development of all the pharyngeal arches and in NCC survival.

The BMP Antagonists Chordin and Noggin Have Essential but Redundant Roles in Mouse Mandibular Outgrowth

Here we investigate the roles of the Bone Morphogenetic Protein (BMP) antagonists Chordin and Noggin in development of the mandible, which is derived from the first branchial arch (BA1). Both genes are expressed in the pharynx during early mandibular outgrowth and later in the mandibular process. Mice mutant for either Nog or Chd have only mild mandibular defects; however, pups of the genotype Chd−/−;Nog+/− exhibit a range of mandibular truncation phenotypes, from normal to agnathia. A few embryos homozygous null for both genes survive to late gestation; many are agnathic, though a few have significant mandibular outgrowth. In mandibular explants, ectopic BMP4 rapidly induces expression of both Chd and Nog, consistent with results obtained in vivo with mutant embryos. Previous work has shown that FGF8 is a survival factor for cells populating the mandibular bud. We find that excess BMP4 represses Fgf8 transcription in mandibular explants. Embryos lacking these BMP antagonists often show a strong reduction in Fgf8 expression in the pharyngeal ectoderm, and increased cell death in the mandibular bud. We suggest that the variable mandibular hypoplasia in double mutants involves increased BMP activity downregulating Fgf8 expression in the pharynx, decreasing cell survival during mandibular outgrowth.

Early gill development in the rainbow trout, Oncorhynchus mykiss.

The morphology of the gills of rainbow trout (Oncorhynchus mykiss) embryos was studied by light and electron microscopy at four different developmental stages. Embryos were examined during gill arch formation (stages 22-24, Vernier, '69), development of the gill filaments (hatching stage), and formation of gill lamellae (stage 36). Our observations showed that the gill arches are covered by endoderm of the pharyngeal pouches and ectoderm of the gill furrows, which meet to form a closing plate. Ultrastructural evidence indicates that secretion of mature hatching gland cells around the closing plates is the mechanism responsible for their perforation and is consistent with the hypothesis of Miller et al. ('93) that cellular reorganization is a major mechanism of initial perforation of closing plates. Epithelia of the gill filaments and gill lamellae are composed of undifferentiated basal epithelial cells, outer pavement cells, and specialized chloride cells and goblet cells. The appearance of these cells and their ultrastructural features during embryonic development are correlated with gill function. It is not until stage 36 that gill epithelia exhibit adultlike ultrastructural features. © 1996 Wiley-Liss, Inc.

Tornwaldt's disease.

Tornwaldt's disease was first described by Tornwaldt as one of the causes of epipharyngitis, and is an inflammation or abscess of the embryonic remnant cyst of the pharyngeal bursa appearing at the posterior median wall of the nasopharynx. Although many cases are symptom-free, symptoms can often be caused by nasal tamponade, trauma, adenotomy, or other mechanical stimuli. Only a few cases have been reported in Japan between 1929 and 1992. At about the 10th week of embryonic development, the pouch, which forms by adhesion of the pharyngeal ectoderm to the notochord at the most cranial end of the notochord, becomes closed at the orifice (cystic type), or crusts adhere to the orifice without closing (crust type). Symptoms are those of upper respiratory tract infection with obstinate occipital pain, purulent choanal discharge, nasal obstruction, halitosis, feeling of ear fullness, clearing of the throat, etc. Posterior rhinoscopy, simple lateral view X-ray tomography, nasopharyngeal fiberoscopy, CT scan and MRI are useful in showing adhesion to the cervical vertebrae. While complete extirpation via a transpalatal approach is desirable, incision or excision of the cyst can also be performed.

Development of glossopharyngeal nerve branches in the early chick embryo with special reference to morphology of the Jacobson's anastomosis

The development of glossopharyngeal nerve branches was studied by an immunohistochemical technique which stains the whole nervous system in situ. Prior to the formation of the ramus (r.) lingualis IX, pre- and post-trematic branches developed just beneath the pharyngeal ectoderm. This mode of development resembled that of the chorda tympani. The post-trematic nerve seemed to be a precursor of the r. lingual. IX. In addition to the r. pharyngeus dorsalis IX, another branch, r. pharyng. posterior IX, appeared. Both these branches formed an anastomosis with the facial and vagus beneath the dorsal aorta. The term Jacobson's anastomosis seemed to be most suitable to refer to an anastomosis made up of these dorsal pharyngeal branches of cranial nerves VII, IX and X. The primary anastomosis between the facial and the glossopharyngeal nerves in the chick is only temporarily present and is comparable to the similar anastomosis in a shark in which the sympathetic system is not present in the cranial region.