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PubMed1986

Tooth induction and temporal patterning in palatal epithelium of fetal mice.

The present study examined the effect of aging on epithelium and on its ability to respond to an inductive stimulus provided by murine dental papillae. In fetal CD-1 mice, 15- to 17-day molar mesenchyme was combined with 15- to 19-day epithelium from the secondary palates. Enamel organs were separated from the dental papillae, and palatal epithelium was peeled away from its underlying mesenchyme after treatment with 1% trypsin. Recombinants of epithelium and papillae were initially cultured on a solidified complex medium for 24 hr followed by an additional 10-14 days of intraocular explanation. Control specimens consisted of isolated molar papillae. Nineteen of 88 isochronal, heterotypic recombinations formed teeth. None of the 46 heterochronal, heterotypic grafts of 18- and 19-day palatal epithelium combined with 15- to 17-day molar papillae-produced teeth. Instead, keratin-filled epithelial cysts and bone spicules were formed. Isolated control molar papillae often formed bone in the intraocular sites but did not form teeth or contain epithelium. These results show that palatal epithelium is first restricted to its developmental pathway at 18 days of gestation. Younger epithelium can convert to functional ameloblasts that secrete enamel protein. In addition to the change in gene expression, normal tooth morphology is attained. The loss of competence of the palatal epithelium at 18 days gestation coincided with the acquisition of stratum corneum and the attainment of the fully differentiated state. The oral surface of palatal epithelium appears to be determined histogenically and morphogenically at 18 days of gestation in mice.

Animals↗
PubMed1990

Expression of the epidermal growth factor receptor in developing fetal mouse palates: an immunohistochemical study.

Epidermal growth factor (EGF) stimulates the growth of various tissues and, therefore, EGF receptor expression in fetal tissues may play a key role in organogenesis. We have examined immunohistochemically the ontogeny and localization of the EGF receptor in the fetal mouse palate during in vivo and in vitro palatogenesis using the anti-human EGF receptor rabbit antibody. Immunoreactive products against the EGF receptor were observed in the palatal tissue examined on days 12, 13, and 14 of gestation. On days 12 and 13, the immunoreactive products were predominantly positive on the oral and medial edge epithelia but were minimal on the epithelium of the vertical shelf. The EGF receptor immunoreactivity was less intense in the posterior palate as compared with the midpalatal region. In the fusing palate of day 14 fetuses, the cells forming the midline epithelial seam were continuously positive for EGF-R immunoreactivity. The mesenchyme of palatal shelves also showed regional heterogeneity and temporal sequence in EGF receptor expression. The localization of the EGF receptor in fetal mouse palates cultured in a serumless medium generally simulated that observed in vivo.

Animals↗
PubMed1990

Toward the origin of the secondary palate. A possible homologue in the embryo of fish, Onchorhynchus kisutch, with description of changes in the basement membrane area.

The oral cavity of embryos and larvae of the teleost Onchorhynchus kisutch was examined. Tissues were obtained at different ages prior to and after hatching and processed for transmission and scanning electron microscopy. A bilaterally symmetrical bulge developed from the superolateral aspect of the oral cavity and projected toward its floor, along the sides of the tongue. The bulge extended from behind the primary palate to a position midway below the eye, anterior to the gill arches, and it is suggested to be the homologue of the secondary palate of higher vertebrates. Ultrastructurally, the epithelium differentiated as the stratified squamous type and it contained mucous cells. However, the features of programmed cell death seen during palatogenesis in mammals were absent in fish. The fish palate mesenchyme, unlike that of higher vertebrates, was chondrified. Also in contrast to higher vertebrates, alterations were seen in the fish palatal basement membrane. A transient appearance of adepidermal granules in the lamina lucida region was followed by organization of collagen fibrils, first into an orthogonal pattern and then into a herring-bone arrangement, in the lamina reticularis region. There was no further advancement in the morphogenesis of fish palate. It is suggested that the differences in the morphogenesis and structure of the secondary palates of various vertebrates may reflect environmentally enforced adaptation, resulting in different programming of cells.

Animals↗
PubMed2003

Combination therapy with folic acid and methionine in the prevention of retinoic acid-induced cleft palate in mice.

BACKGROUND: During formation of the secondary palate, clefting may result when critical developmental events are altered. The purpose of this study was to reduce the incidence of retinoic acid (RA)-induced cleft palate (CP) in mice by the co-administration of folic acid (FA), methionine (ME) or a combination of both. METHODS: Four groups of time-pregnant Swiss Webster mice were injected intraperitoneally with 50 mg/kg RA on gestational day (GD) 10. Likewise, 4.0 mg/kg FA and 187 mg/kg ME were administered on GD 8-11. The experiment included a control group (RA plus H2O) and three experimental groups, (RA plus therapeutic doses of FA, ME, or FA + ME). Necropsies were carried out on GD 18 and pups were analyzed for teratogenic effects. RESULTS: Litters that received no therapy exhibited 100% CP with individual pups showing 76% susceptibility. Each therapy administered separately reduced the frequency of CP to approximately 6%, and the combination of FA and ME completely prevented the occurrence of RA-induced cleft palate (0%). A second experiment was conducted in which therapy levels were decreased by 25%. Litters that did not receive therapy experienced 100% clefting and individual pups exhibited CP at 86%. These therapies administered separately did not alter significantly the frequency of cleft palate. The combined doses of FA and ME, however, lowered significantly the frequency of cleft palate to 46%. Decreases in limb and tail defects with FA + ME therapy were also observed in both experiments. CONCLUSIONS: Although FA and ME, at appropriate levels, can reduce individually the frequency of RA-induced cleft palate and other defects in mice, the results from the present study suggest that there is an additive interaction between the two therapeutic agents that can reduce further the teratogenic impact of RA. Further studies are needed to assess the mechanism of action of concomitant doses of FA and ME in the reduction of drug-induced birth defects.

Abnormalities, Drug-Induced↗
PubMed2006

Inhibition of SMAD2 expression prevents murine palatal fusion.

Transforming growth factor (TGF)-beta 3 is known to regulate the disappearance of murine medial edge epithelium (MEE) during palatal fusion. Our previous studies showed that SMAD2, a TGF-beta signaling mediator, was expressed and phosphorylated primarily in the MEE and that SMAD2 phosphorylation in the MEE was temporospatially regulated by TGF-beta 3. The goal of this study was to examine the requirement for SMAD2 to complete the developmental events necessary for palatal fusion. SMAD2 expression was inhibited with Smad2 siRNA transfection into palatal tissues in vitro. The results showed that Smad2 siRNA transfection resulted in the maintenance of MEE cells in the palatal midline. Western blot and immunofluorescence analyses confirmed that the endogenous SMAD2 and phospho-SMAD2 levels were reduced following siRNA transfection. The SMAD3 level was not altered by the Smad2 siRNA transfection. The persistence of the MEE and the decreased SMAD2/phospho-SMAD2 levels were coincident with increased MEE cell proliferation. Addition of exogenous TGF-beta 3 increased p-SMAD2 level but not the total SMAD2 level. Therefore, exogenous TGF-beta 3 was not able to induce p-SMAD2 enough to rescue the palatal phenotype in the Smad2 siRNA group. The results indicated that the endogenous SMAD2 level is crucial in the regulation of disappearance of MEE during palatal fusion.

Animals↗
PubMed1994

Effects of 5-fluorouracil on macromolecular synthesis during secondary palate development in quail.

A study was undertaken to examine the growth of normal and 5-fluorouracil-treated quail secondary palate during embryogenesis. The rates of DNA, RNA, and protein synthesis were measured in the developing quail palate by liquid scintillation counting of radiolabelled thymidine, uridine, or leucine. In addition, shelf volume was determined morphometrically. The results showed that in control palates the shelf volume increased rapidly between days 5 and 7 of incubation. Drug treatment on day 4 did not alter the shelf volume until day 9 of incubation, at which time the treated shelves were smaller than controls. In control palates, the rate of DNA synthesis decreased steadily between days 5 and 9 of incubation. A burst in RNA synthesis on day 7 of incubation was followed by an increase in protein synthesis. Administration of FU seems to exert its effect via disturbing the synthesis of RNA and protein, instead of disruption of DNA synthesis, to ultimately affect the shelf area, and thus palate morphogenesis in quail. Comparison of avian and mammalian data indicated that differences in their palate morphogenesis are also reflected in the different temporal patterns of various macromolecular synthesis.

Animals↗
PubMed1986

Mechanical factors in the evolution of the mammalian secondary palate: a theoretical analysis.

The secondary palate of mammals is a bony shelf that closes the ventral aspect of the rostrum. The rostrum, therefore, approximates to a tapered semicylindrical tube that is theoretically a mechanically efficient structure for resisting the forces of biting, including the more prolonged bouts of mastication typical of mammals. Certain mammal-like reptiles illustrate stages in the development of the palate in which the shelves projecting medially from each premaxilla and maxilla do not meet in the midline. We evaluate several geometric properties of sections through the rostrum of the American opossum (Didelphis virginiana). For loading at the incisors and canines, these properties indicate the structural strength and stiffness in both bending and torsion of the rostrum and of single maxillae. We then repeat the analysis but progressively omit segments of the palatal shelf, a procedure which simulates, in reverse, the evolutionary development of the structure. The results demonstrate that the secondary palate contributes significantly to the torsional strength and stiffness of the rostrum of Didelphis and to the strength of each maxilla in lateromedial bending. The major evolutionary implications of the results are that the rapid increase in rostral strength with small increments of the palatal shelves may have been a significant factor in the development of the complete structure. The results indicate that there was a marked jump in torsional strength and stiffness when the shelves met in the midline, which is likely to have been important in the subsequent development of the diverse masticatory mechanisms of cynodonts and mammals. On the basis of this analysis the mammalian secondary palate may be interpreted as one of a number of methods, seen in the mammal-like reptiles, for strengthening the rostrum.

Animals↗
PubMed1977

Ultrastructure of the expected fusion zone in rat fetuses with diazo-oxo-norleucine (DON)-induced cleft palate.

The aim of this study was to determine whether the glutamine analog, 6-diazo-5-oxo-L-norleucine (DON), which is known to inhibit cell degeneration in rat palatal processes in vitro, exerted a similar effect on cleft palatal processes in vivo. Sprague-Dawley rats were injected intraperitoneally with 5.0 mg/kg body wt of DON on Day 15 of gestation and fetuses were removed over Days 16, 17 and 18. A high frequency (80-90%) of cleft palate was obtained. Fetal heads were removed on each of the three days and transverse sections of the palatal processes were examined by light and electron microscopy. Results showed that treatment with DON failed to inhibit degenerative changes in the palatal epithelium. The same sequence and timing of ultrastructural changes occurred in the expected fusion zone (EFZ) as have been described previously in cleft palatal processes from Meclozine-treated and amniotic sac punctured rat fetuses; namely, autophagic cytoplasmic degeneration, loss of basal lamina and the subepithelial accumulation of macrophages all of which were most prominent in that part of the EFZ immediately next to the developing oral epithelium. The results therefore suggest that a teratogenic dose of DON does not interfere with the ultrastructurally observable changes in the EFZ.

Abnormalities, Drug-Induced↗
PubMed1982

Susceptibility to cleft palate and the major histocompatibility complex (H-2) in the mouse.

The congenic mouse strains B10 and B10.A differ genetically only at the H-2 locus, B10 having the H-2b and B10.A the H-2a haplotype. The two strains also differ in susceptibility to cortisone-induced cleft palate, B10 being more resistant than B10.A. Since stage of palate closure is also associated with susceptibility to cortisone-induced cleft palate it was postulated that the H-2 haplotype may affect the cortisone-induced cleft palate susceptibility by altering the stage of palate closure. The present study shows that palate closure occurs at the same stage in the two strains, so this hypothesis must be rejected.

Animals↗
PubMed1986

Synergistic interaction of 2,3,7,8,-tetrachlorodibenzo-p-dioxin and hydrocortisone in the induction of cleft palate in mice.

Glucocorticoids cause cleft palate in sensitive mouse strains by interfering with the proliferation of mesenchymal cells in the palatal shelves; 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) also causes cleft palate, but its effects involve the epithelial cells. The purpose of this study was to examine the interaction of TCDD and the glucocorticoid hydrocortisone in the induction of malformations. Pregnant C57BL/6N mice were treated on gestation days 10-13 with TCDD (0 or 3 micrograms/kg, p.o.), hydrocortisone (0, 25, 50, or 100 mg/kg, s.c.) or a combination of TCDD and hydrocortisone. The dams were killed on gestation day 18 and the mice were analyzed for maternal and fetal toxicity and soft tissue malformations. TCDD alone had no effect on litter size, fetal weight or viability, or maternal weight gain. This dose of TCDD is essentially a threshold dose and it did not produce cleft palate in this study, but all the TCDD-treated fetuses had hydronephrosis, the most sensitive indicator of TCDD teratogenicity. Hydrocortisone alone caused dose-related decreases in fetal weight and maternal liver/body weight ratios, and dose-related increases in cleft palate (0, 5, 10, and 30%). No effects of hydrocortisone were detected on litter size or fetal viability, but maternal weights were affected. Combination of all doses of hydrocortisone with TCDD resulted in a 100% incidence of cleft palate, accompanied by a decrease in litter size and fetal weight and an increase in fetal mortality related to the dose of hydrocortisone. TCDD tended to reverse the decrease in liver/body weight ratio seen with hydrocortisone alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Drug-Induced↗
PubMed1988

Vertical development of the secondary palate in hamster embryos following exposure to 6-mercaptopurine.

Cellular aspects of vertical development of the secondary palate were examined in control and 6-mercaptopurine (6MP)-treated hamster embryos. Cross-sectional area of the palatal shelf was measured and the numbers of both epithelial and mesenchymal cells counted. Also, in 6MP-treated palates the damaged mesenchymal cells, characterized by the presence of dense bodies, were counted. DNA synthesis in both control and treated fetuses was measured by 3H-thymidine incorporation. The results indicated that both the shelf area and cell numbers increased with age in control and 6MP-treated palates. However, in controls the mesenchymal cell density and DNA synthesis showed two peaks that were absent following 6MP treatment. Unlike controls, in treated embryos the damage to mesenchymal cells became increasingly pronounced between days 10:00 and 10:12 but subsided by day 11:00 of gestation. It is suggested that a major force in the development of the initial primordia and early vertical development of the palatal shelf may be provided by a spurt of DNA synthesis in the mesenchymal cells resulting in their increased number. After 6MP treatment, depression of DNA synthesis and consequent reduction in the mesenchymal cell number and density followed by cell damage lead to retardation in the vertical development of the palatal shelves.

Animals↗
PubMed1994

Ah receptor in embryonic mouse palate and effects of TCDD on receptor expression.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is the most potent member of a family of halogenated aromatic hydrocarbons which are widespread environmental contaminants. In animals the adverse biological effects of TCDD include carcinogenesis, reproductive toxicity, immune function alteration, hyperkeratosis, hepatotoxicity, thymic involution, and teratogenesis. In the mouse embryo, TCDD induces cleft palate through a mechanism which involves altered differentiation and proliferation of the palatal cells, resulting in the failure of opposing shelves to fuse. Cleft palate induction by TCDD requires the Ah receptor. This study examines the expression of the Ah receptor in secondary palate of control and TCDD-exposed C57BL/6N embryos using in situ hybridization, Northern blots, and immunohistochemistry. Ah receptor protein expression was significantly higher in epithelial versus mesenchymal cells, and regional differences in expression within the epithelium were statistically significant. TCDD exposure was shown to downregulate Ah receptor mRNA and protein throughout the palatal shelf and this occurred at both the teratogenic dose and the dose which was not sufficient to produce cleft palate. This study represents the first demonstration of the tissue and cellular localization of the Ah receptor, raising questions about the extrapolation of results from cultured tumor cells to those observed in vivo.

Animals↗
PubMed2000

Secalonic acid D alters the nature of and inhibits the binding of the transcription factors to the phorbol 12-O-tetradecanoate-13 acetate-response element in the developing murine secondary palate.

Secalonic acid D (SAD), a mycotoxin produced by Penicillium oxalicum in corn, induces cleft palate (CP) in the offspring of exposed dams. Results of recent studies suggest that protein kinase C (PKC) inhibition by SAD may be relevant to its CP-induction. Downstream effects of PKC are determined by the nature of transcription factors (TF) that form the activator protein-1 (AP-1) and the binding of AP-1 (and other TF) to the phorbol 12-O-tetradecanoate-13 acetate-response element (TRE) to form AP-1-TRE complex, neither of which have been studied in the palate. The aims of the present study were to identify the components of the murine palatal AP-1-TRE complex during development and to uncover the effects of SAD on this complex. Western blots and gel mobility shift assays of control palatal nuclear extracts revealed that, although all relevant TF are present in the palate throughout development, only cyclic-AMP response element (CRE) binding protein (CREB) and CRE-modulator protein-1 (CREM-1) and activating transcription factor-1 bound to TRE on Gestation Day (GD) 12. The pattern shifted to c-Jun and c-Fos (known AP-1 components) on GD 13 and 14. In SAD-treated offspring, however, CREM-1 alone; c-Jun, c-Fos, and CREB; and c-Jun and c-Fos bound to TRE on GD 12, 13, and 14, respectively. Binding of TF to TRE was inhibited by SAD on both GD 12 and 13. These results suggest that a dynamic shift in the binding of TF to TRE from PKA- to PKC-responsive TF occurs during palate development and that teratogens such as SAD can alter both the nature and extent of TF binding to TRE.

Animals↗
PubMed1993

Rapid changes in the extracellular matrix accompany in vitro palatal shelf remodelling.

The sequence of events and the distribution of extracellular matrix (ECM) components was examined during mouse secondary palatal shelf elevation in an in vitro model using standard roller tube culture methods developed for the culture of early embryos. In this culture system, the morphological changes associated with remodelling and reorientation of the palatal shelves of gestational day 13 mouse fetuses were similar to those observed in vivo. However, in specimens explanted 24-30 h prior to reorientation in vivo, remodelling began rapidly after explantation, and significant reorientation was accomplished within 4 h. Midline contact between the shelves did not occur until after 18 h in vitro, concomitant with shelf growth. Therefore, in this in vitro model, events related to palatal shelf remodelling and reorientation can be distinguished from those related to shelf growth. We used this in vitro model to characterize the transient changes in ECM distribution and accumulation that occur concomitant with events in shelf remodelling. Our results show that, during rapid remodelling in vitro, the relative distributions of collagen III, fibronectin and hyaluronate, as visualized by immunofluorescent staining, decreased within specific regions of the mesenchymal compartment. In contrast, the distribution of collagen I within the mesenchyme increased, and the distribution of tenascin did not change significantly. All molecules examined, except tenascin, showed changes in distribution within the basement membrane. These patterns of distribution are similar to those observed during more gradual remodelling in vivo. During remodelling in vitro, the deposition of [3H]-glucosamine- and [3H]-proline-labelled components of the ECM, as visualized by autoradiography, was greatest during the first 3 h of culture. During this period, labelled ECM accumulated within specific regions of the mesenchyme and palatal epithelial basement membrane. Uptake was reduced dramatically during the subsequent 3 h in culture and was restricted mainly to the palatal epithelium and its underlying basement membrane. The in vitro system permitted the characterization of early events in shelf remodelling leading to reorientation. Results suggest that remodelling is accompanied by rapid, local accumulation of ECM in specific regions of the palatal shelf previously thought to play a role in the process.

Animals↗
PubMed1991

Excitation and inhibition of trigeminal motoneurons by palatal stimulation.

Excitation and inhibition of jaw-closing motoneurons (Masseteric and Temporal Motoneurons, Mass. and Temp. Mns) during transient jaw closing, the so-called jaw-closing reflex, and prolonged jaw opening elicited by palatal stimulation were studied. By pressing the anterior palatal surfaces sustained jaw opening was elicited, suggesting that sustained jaw opening results from inhibition of tonic background activity of jaw-closing motoneurons by inhibitory postsynaptic potentials (IPSPs) elicited by mechanical stimulation of the anterior palatal mucosa. Recordings showed that the onset of IPSPs was 80 ms earlier than the onset of jaw opening. Application of diffuse pressure stimulation to the posterior palatal surfaces elicited bursts of spikes triggered on excitatory postsynaptic potentials (EPSPs), suggesting that mechanosensory receptors from the posterior palatal mucosa send excitatory synaptic inputs to jaw-closing motoneurons. Furthermore, it is suggested that mechanosensory inputs from the posterior palatal mucosa may excite neurons in the central pattern generator and provide the motor patterns responsible for jaw closure during the jaw-closing reflex. We have demonstrated that excitation of Mass. Mns innervating the deep masseter muscle mainly contributed to maintaining the occlusal phase of jaw closure during the jaw-closing reflex. However, the onset of EPSPs was 100 to 160 ms (n = 27) earlier than the onset of jaw closure. In studies on spontaneously occurring jaw closure it was demonstrated that there was a proportional increase in the number of spikes of the Temp. Mn and the mechanical response (jaw closure).

Animals↗
PubMed1995

Organization of the intercellular spaces of porcine epidermal and palatal stratum corneum: a quantitative study employing ruthenium tetroxide.

Previous studies have demonstrated that the intercellular spaces of the stratum corneum contain multilamellar lipid sheets with variable ultrastructure in addition to desmosomes or desmosomal remnants. The intercellular lamellae are thought to provide a permeability barrier whereas the desmosomes are responsible for cell-cell cohesion. In this study, transmission electron microscopy of RuO4-fixed tissue was used to compare the proportions of the intercellular spaces in epidermal and palatal stratum corneum occupied by desmosomes and by different patterns of lamellae. Desmosomes are more abundant in palatal than in epidermal stratum corneum (46.9 vs 15.0% length of intercellular space). In epidermis the most frequent lamellar arrangements involve 3 (23.5%) or 6 (24.2%) lucent bands with an alternating broad-narrow-broad pattern, whereas the most frequent lamellar arrangements in palatal tissue are 2 (17.2%) or 4 (10.5%) lucent bands of uniform width. Most of the nondesmosomal portion of the intercellular space in palatal stratum corneum was dilated and had elongated lamellae at the periphery and short disorganized lamellae and amorphous electron-dense material in the interior. It is concluded that the multilamellar lipid sheets are less extensive in palatal than in epidermal stratum corneum, which could explain the greater permeability of the palate.

Animals↗
PubMed1975

Ultrastructures of glosso-palatal fusion after treatment of meclozine-hydrochloride.

The behavior of the epithelial cells on the tongue and palatal processes during glosso-palatal fusion induced by Meclozine-hydrochloride was investigated with light and electron microscopes. Microscopical observations revealed that; at two or three days after the administration, the palatal processes were approximating to the tongue, and the superficial cells on the lateral sides of tongue became swollen and to have inclusion bodies, and in the epithelium on the medial sides of palatal processes, some inclusion bodies appeared too. At the time of contact, the superficial epithelial cells of tongue tended to degenerate markedly, and these degenerating cells were dissociated from the epithelium, and concurrently, superficial layer of the palatal epithelium became to have a lot of inclusion bodies. Between the two tissues, attachment devices developed just after the contact, and then, the cells in the intervening epithelial lining fell into a degeneration gradually. As well known, Meclozine-hydrochloride is one of important miner tranquilizers. From the findings mentioned above, it seemed to be possible that a heterotopic fusion caused with this drug is a result of a destruction of embryonic epithelium on tongue and palatal processes at a certain stage of development.

Animals↗
PubMed1985

Histochemical localization of glycosaminoglycans during morphogenesis of the secondary palate in mice.

The hydration of hyaluronic acid (HA) accumulated in the secondary palatal processes is expected to exert an intrinsic tissue pressure that could, in part, provide the impetus for shelf reorientation. Glycosaminoglycans were histochemically localized in the A/J mouse palate during development (days 12 to 15) by specific enzymatic degradation followed by preferential staining with alcian blue under differential pH or MgCl2 concentration. The presence of HA and chondroitin sulphates A and C (CS) was demonstrated in proportions that differed regionally. At the time of reorientation (days 14 to 15) HA was the predominant staining component, being distributed according to the relative prominence of extracellular spaces (ECS). HA was present in higher concentration in the anterior than the posterior part of the palate, particularly in an area of low cell density adjoining the CS-rich mesenchyme of the maxillary process. This arrangement suggests that the maxillary process might provide a resilient incompressible structural base for the palate as its HA-rich ECS expands. Sulphated GAG, with CS being the predominant component, was localized for the most part on the oral-side mesenchyme both in the anterior and posterior palate. The most intense staining of sulphated proteoglycans occurred in association with the basal lamina along the presumptive oral-side. Mesenchymal cells along this region appeared condensed and may have been stabilized by these sulphated GAG providing structural constraints which might function in palate morphogenesis.

Animals↗