Primary Palate Formation Research Articles

Growth and primary palate formation of mouse embryos in culture

Growth and primary palate formation of mouse embryos in culture

Rapid nasal pit formation in mouse embryos stimulated by ATP-containing medium.

The primary palate in the mouse is composed of epithelium and mesenchyme. Most studies on primary palate formation have concentrated on the role of the mesenchyme based upon the hypothesis that mesenchymal accumulation elevated the sides of the nasal placodes, thereby creating the depressed nasal pits. This study demonstrates that the epithelium is actively participating in formation of the nasal pits. Mouse heads from embryos of 14 to 24 paris of body somites were placed in medium 199 and photographed. The medium was replaced with medium containing 1.0 mM ATP and 0.05% Triton-X. Within 5 minutes, the placodes either thickened or invaginated. Control heads exposed to medium 199 containing only Triton-X or ATP did not show any invaginations. The rapid thickening and invagination stimulated by ATP-containing medium demonstrates that the epithelium is the dominant tissue in nasal put formation. Although mesenchymal accumulation certainly contributes to the formation of the primary palate, it is the placodal epithelial invagination that appears to shape the nasal pits.

Developmental aspects of primary palate formation (author's transl)

Developmental aspects of primary palate formation (author's transl)

Autoradiographic study of macromolecular synthesis in the fusion epithelium of the developing rat primary palatein vitro

The facial processes involved in primary palate formation undergo epithelial fusion in a manner morphologically analogous to that observed during secondary palate formation. We have used whole embryo culture to analyze the synthesis of macromolecules (DNA, protein glycoprotein) in the primary palate, based on the incorporation of various labeled precursors. The results of this study demonstrate that changes in the synthesis of macromolecules occur during the fusion of the facial processes, which resemble those previously reported to occur during secondary palate development. These changes include cessation of DNA synthesis in cells in a restricted zone of the epithelium, concomitant with maintenance of glycoprotein synthesis. These findings indicate that the molecular events underlying the development of the primary and secondary palate may be similar.

Facial development in normal and mutant chick embryos. I. Scanning electron microscopy of primary palate formation.

Early facial development in normal chick embryos was studied by scanning electron microscopy, and compared to the abnormal facial development of a mutant in which primary palate formation does not occur, thus resulting in bilateral cleft lip. In both normal and "cleft primary palate" mutant embryos, subsequent to the appearance of the nasal placodes, the surrounding tissues elevate to give rise to the presumptive facial primordia. As the facial primordia grow forward, they gradually assume the configuration of a square which is most pronounced at five days development. In normal embryos, the square configuration is then lost as the facial primordia become aligned in preparation for primary palate formation. The primary palate is formed at six days development by fusion of the "free-ended" medial nasal processes with the combined lateral nasal and maxillary processes across the nasal grooves. Just prior to fusion, long, slender filaments extend from the apposing surfaces of the facial primordia in the regions of prefusion contact. It is speculated that these "prefusion filaments" may function in alignment or adhesion of the facial primordia. In "cleft primary palate" embryos, facial morphogenesis appears to arrest at five days development, so that the square configuration persists. The medial nasal processes never contact the lateral nasal and maxillary processes, but instead remain separated from them by wide nasal grooves. Furthermore, facial primordia of mutant embryos do not exhibit the "prefusion filaments" characteristic of normal embryos.

Cell proliferation during morphogenetic change; analysis of frontonasal morphogenesis in the chick embryo employing DNA labeling indices

ABSTRACT The role of cell proliferation was analyzed in the chick embryo system employing DNA labeling indices during the invagination of the olfactory placode and the development of the lateral and medial nasal processes. Chick embryos were labeled for 1 h with [3H]thymidine and processed histologically and autoradiographically. The percentage of labeled mesenchymal cells in delineated areas within and adjacent to the nasal processes was determined. From analysis of labeling indices of each area at successive developmental stages, it was concluded that cell proliferation of mesenchyme, as measured by DNA labeling indices, did not appear to increase during the formation of the nasal processes, and that cell proliferation actually declined during the later stages of nasal process formation. Differences were also found between the labeling indices of the mesenchyme of the nasal processes as compared to that of adjacent areas. These differences tended to become greater as development progressed. In all of the areas studied, cell proliferation declined during the later stages of development but the magnitude of the decline was greater in the areas adjacent to the nasal processes. Differential rates of decline, rather than acceleration of cell proliferation, therefore, appears to be operative as a morphogenetic mechanism during early primary palate formation.

Concanavalin A binding to the epithelial surface of the developing mouse olfactory placode.

Concanavalin A (Con A), a lectin binding to mannosyl and glucosyl residues of glycoproteins and glycolipids, was used to study the appearance of carbohydrate-rich cell surface material on the olfactory placode and nasal processes which contribute to formidine was also used in an attempt to correlate changes in labeling index with formation of the olfactory placode and nasal processes. The cell surface of the early frontonasal epithelium binds Con A very little, if at all, but Con A binding was observed when the olfactory placode could be identified as a plate of cuboidal cells that exhibited a reduced labeling index. During the period of formation of the nasal processes, Con A binding was observed on the facial epithelium including the presumptive contact region. There was also a decline in the labeling index throughout primary palate formation. This study provides three criteria by which the olfactory placode can be identified: a morphological change of placode cells to a cuboidal shape, a synthesis or rearrangement of surface coat material that binds Con A, and a reduced labeling index.