scholarly journals Spatially restricted dental regeneration drives pufferfish beak development

2017 ◽  
Vol 114 (22) ◽  
pp. E4425-E4434 ◽  
Author(s):  
Alexandre P. Thiery ◽  
Takanori Shono ◽  
Daisuke Kurokawa ◽  
Ralf Britz ◽  
Zerina Johanson ◽  
...  
Keyword(s):  
First Generation ◽  
Lineage Tracing ◽  
Oral Epithelium ◽  
Dental Morphology ◽  
Tooth Replacement ◽  
Evolution And Development ◽  
Dental Epithelium ◽  
Dramatic Shift ◽  
Progressive Accumulation ◽  
Microct Analysis

Vertebrate dentitions are extraordinarily diverse in both morphology and regenerative capacity. The teleost order Tetraodontiformes exhibits an exceptional array of novel dental morphologies, epitomized by constrained beak-like dentitions in several families, i.e., porcupinefishes, three-toothed pufferfishes, ocean sunfishes, and pufferfishes. Modification of tooth replacement within these groups leads to the progressive accumulation of tooth generations, underlying the structure of their beaks. We focus on the dentition of the pufferfish (Tetraodontidae) because of its distinct dental morphology. This complex dentition develops as a result of (i) a reduction in the number of tooth positions from seven to one per quadrant during the transition from first to second tooth generations and (ii) a dramatic shift in tooth morphogenesis following the development of the first-generation teeth, leading to the elongation of dental units along the jaw. Gene expression and 1,1′-Dioctadecyl-3,3,3′,3′-tetramethylindocarbocyanine perchlorate (DiI) lineage tracing reveal a putative dental epithelial progenitor niche, suggesting a highly conserved mechanism for tooth regeneration despite the development of a unique dentition. MicroCT analysis reveals restricted labial openings in the beak, through which the dental epithelium (lamina) invades the cavity of the highly mineralized beak. Reduction in the number of replacement tooth positions coincides with the development of only four labial openings in the pufferfish beak, restricting connection of the oral epithelium to the dental cavity. Our data suggest the spatial restriction of dental regeneration, coupled with the unique extension of the replacement dental units throughout the jaw, are primary contributors to the evolution and development of this unique beak-like dentition.

Cranial and dental morphology in a bohaiornithid enantiornithine with information on its tooth replacement pattern

2021 ◽  
pp. 105021
Author(s):  
Di Liu ◽  
L.M. Chiappe ◽  
Becky Wu ◽  
Qingjin Meng ◽  
Yuguang Zhang ◽  
...  
Keyword(s):  
Dental Morphology ◽  
Tooth Replacement ◽  
Replacement Pattern

Tissue interactions in embryonic mouse tooth germs

Development ◽  
1970 ◽  
Vol 24 (1) ◽  
pp. 159-171
Author(s):  
Edward J. Kollar ◽  
Grace R. Baird
Keyword(s):  
Enamel Organ ◽  
Oral Epithelium ◽  
Embryonic Mouse ◽  
Tooth Shape ◽  
Structural Specificity ◽  
Dental Papilla ◽  
Tissue Interactions ◽  
Dental Epithelium ◽  
Tooth Germs

The ability of fragments of incisor enamel organ and lip-furrow epithelium from 15- and 16-day old embryonic mice to regulate into harmonious tooth constructions is described. The cervical loop and upper half portions of the incisor enamel organ were confronted with incisor or molar dental papillae. Similar combinations were made from lip-furrow epithelium and incisor or molar papillae. The cultures were grown in the anterior chambers of homologous host eyes. The epithelial fragments from the incisor enamel organ when associated with the dental papillae reconstruct teeth typical in all respects; enamel and dentin matrices are deposited. Lip-furrow epithelium arises from the oral epithelium and is temporally and spatially related to the incisor dental epithelium proper. This ectopic epithelium was confronted by incisor and molar papillae. Harmonious teeth developed in these explants. It is concluded that the ability of the dental papillae to elicit new cytodifferentiative and biochemical syntheses from the lip-furrow epithelium indicates that the dental papillae act inductively during tooth ontogeny. The shape of the teeth reconstructed from enamel organ fragments and lip-furrow epithelium were incisiform or molariform in response to the incisor or molar dental papillae. These data confirm the conclusion that the structural specificity for tooth shape resides in the dental papilla.

scholarly journals Ameloblastin is a cell adhesion molecule required for maintaining the differentiation state of ameloblasts

2004 ◽  
Vol 167 (5) ◽  
pp. 973-983 ◽  
Author(s):  
Satoshi Fukumoto ◽  
Takayoshi Kiba ◽  
Bradford Hall ◽  
Noriyuki Iehara ◽  
Takashi Nakamura ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Matrix Protein ◽  
Oral Epithelium ◽  
Enamel Matrix Protein ◽  
Mineralized Tissues ◽  
The Matrix ◽  
A Cell ◽  
Dental Epithelium

Tooth morphogenesis results from reciprocal interactions between oral epithelium and ectomesenchyme culminating in the formation of mineralized tissues, enamel, and dentin. During this process, epithelial cells differentiate into enamel-secreting ameloblasts. Ameloblastin, an enamel matrix protein, is expressed by differentiating ameloblasts. Here, we report the creation of ameloblastin-null mice, which developed severe enamel hypoplasia. In mutant tooth, the dental epithelium differentiated into enamel-secreting ameloblasts, but the cells were detached from the matrix and subsequently lost cell polarity, resumed proliferation, and formed multicell layers. Expression of Msx2, p27, and p75 were deregulated in mutant ameloblasts, the phenotypes of which were reversed to undifferentiated epithelium. We found that recombinant ameloblastin adhered specifically to ameloblasts and inhibited cell proliferation. The mutant mice developed an odontogenic tumor of dental epithelium origin. Thus, ameloblastin is a cell adhesion molecule essential for amelogenesis, and it plays a role in maintaining the differentiation state of secretory stage ameloblasts by binding to ameloblasts and inhibiting proliferation.

scholarly journals Dentition and feeding in Placodontia: tooth replacement in Henodus chelyops

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yannick Pommery ◽  
Torsten M. Scheyer ◽  
James M. Neenan ◽  
Tobias Reich ◽  
Vincent Fernandez ◽  
...  
Keyword(s):  
Phylogenetic Position ◽  
Single Pair ◽  
Dental Morphology ◽  
Tooth Replacement ◽  
Dental Wear ◽  
Phylogeny Analysis ◽  
Synchrotron Tomography ◽  
The Matrix ◽  
Size And Morphology ◽  
Central Cusp

Abstract Background Placodontia is a Triassic sauropterygian reptile group characterized by flat and enlarged crushing teeth adapted to a durophagous diet. The enigmatic placodont Henodus chelyops has numerous autapomorphic character states, including extreme tooth count reduction to only a single pair of palatine and dentary crushing teeth. This renders the species unusual among placodonts and challenges identification of its phylogenetic position. Results The skulls of two Henodus chelyops specimens were visualized with synchrotron tomography to investigate the complete anatomy of their functional and replacement crushing dentition in 3D. All teeth of both specimens were segmented, measured, and statistically compared to reveal that H. chelyops teeth are much smaller than the posterior palatine teeth of other cyamodontoid placodonts with the exception of Parahenodus atancensis from the Iberian Peninsula. The replacement teeth of this species are quite similar in size and morphology to the functional teeth. Conclusion As other placodonts, Henodus chelyops exhibits vertical tooth replacement. This suggests that vertical tooth replacement arose relatively early in placodont phylogeny. Analysis of dental morphology in H. chelyops revealed a concave shape of the occlusal surface and the notable absence of a central cusp. This dental morphology could have reduced dental wear and protected against failure. Hence, the concave teeth of H. chelyops appear to be adapted to process small invertebrate items, such as branchiopod crustaceans. Small gastropods were encountered in the matrix close to both studied skulls.

scholarly journals Requirement of Irf6 and Esrp1/2 in frontonasal and palatal epithelium to regulate craniofacial and palate morphogenesis in mouse and zebrafish

2020 ◽  
Author(s):  
Shannon H. Carroll ◽  
Claudio Macias Trevino ◽  
Edward B-H Li ◽  
Kenta Kawasaki ◽  
Nora Alhazmi ◽  
...  
Keyword(s):  
Cell Population ◽  
Mouth Opening ◽  
Embryonic Cell ◽  
Lineage Tracing ◽  
Oral Epithelium ◽  
Triple Mutant ◽  
Cranial Neural Crest Cells ◽  
Future Work ◽  
Insight Into ◽  
Morphogenetic Analysis

ABSTRACTOrofacial clefts are among the most common human congenital malformations. Irf6 and Esrp1 are two key genes important for palate development, conserved across vertebrates. In the zebrafish, we found that irf6 regulates the expression of esrp1. Using RNAscope, we detailed overlapping Irf6 and Esrp1/2 gene expression in the mouse frontonasal prominence ectoderm, lambda joint periderm, palate and lip epithelium. In the zebrafish, irf6 and esrp1/2 share expression in the pre-gastrulation periderm and the embryonic frontonasal ectoderm, oral epithelium ventral to the anterior neurocranium (ANC), and the developing stomodeum. Genetic disruption of irf6 and esrp1/2 in the zebrafish resulted in cleft of the ANC. In the esrp1/2 zebrafish mutant, cleft of the mouth opening formed and appeared to tether into the ANC cleft. Lineage tracing of the anterior cranial neural crest cells revealed that cleft of the ANC resulted not from migration defect, but from impaired chondrogenesis. Molecular analysis of the aberrant cells localized within the ANC cleft revealed that this cell population espresses sox10, col1a1 and irf6 and is adjacent to cells expressing epithelial krt4. Detailed morphogenetic analysis of mouse Irf6 mutant revealed mesenchymal defects not observed in the Esrp1/2 mutant. Analysis of breeding compound Irf6;Esrp1;Esrp2 mutant suggests that these genes interact where the triple mutant is not observed. Taken together, these studies highlight the complementary analysis of Irf6 and Esrp1/2 in mouse and zebrafish models and captured an unique aberrant embryonic cell population that contributes to cleft pathogenesis. Future work characterizing this unqiue sox10+, col1a1+, irf6+ cell population will yield additional insight into cleft pathogenesis.

Epithelial-mesenchymal interactions are required for msx 1 and msx 2 gene expression in the developing murine molar tooth

Development ◽  
1993 ◽  
Vol 117 (2) ◽  
pp. 461-470 ◽  
Author(s):  
A.K. Jowett ◽  
S. Vainio ◽  
M.W. Ferguson ◽  
P.T. Sharpe ◽  
I. Thesleff
Keyword(s):  
Gene Expression ◽  
Tooth Development ◽  
Homeobox Gene ◽  
Oral Epithelium ◽  
Tooth Formation ◽  
Dental Papilla ◽  
Tissue Interactions ◽  
Dental Epithelium

Duplication of the msh-like homeobox gene of Drosophila may be related to the evolution of the vertebrate head. The murine homologues of this gene, msx 1 and msx 2 are expressed in the developing craniofacial complex including the branchial arches, especially in regions of epithelial-mesenchymal organogenesis including the developing tooth. By performing in vitro recombination experiments using homochronic dental and non-dental epithelial and mesenchymal tissues from E10 to E18 mouse embryos, we have found that the maintenance of homeobox gene expression in the tooth is dependent upon tissue interactions. In homotypic recombinants, dental-type tissue interactions occur, leading to expression of both genes in a manner similar to that seen during in vivo development. msx 1 is expressed exclusively in mesenchyme, both in the dental papilla and follicle. msx 2 is expressed in the dental epithelium and only in the mesenchyme of the dental papilla. In heterotypic recombinants, the dental epithelium is able to induce msx 1 expression in non-dental mesenchyme, this potential being lost at the bell stage. In these recombinants msx 2 was induced by presumptive dental epithelium prior to the bud stage but not thereafter. The expression of msx 1 and msx 2 in dental mesenchyme requires the presence of epithelium until the early bell stage. However, whereas non-dental, oral epithelium is capable of maintaining expression of msx 1 in dental mesenchyme throughout tooth development, induction of msx 2 was temporally restricted suggesting regulation by a specific epithelial-mesenchymal interaction related to the inductive events of tooth formation. msx 1 and msx 2, as putative transcription factors, may play a role in regulating the expression of other genes during tooth formation. We conclude that expression of msx 1 in jaw mesenchyme requires a non-specific epithelial signal, whereas msx 2 expression in either epithelium or mesenchyme requires reciprocal interactions between specialized dental cell populations.

Associations between transforming growth factor beta 1 RNA expression and epithelial-mesenchymal interactions during tooth morphogenesis

Development ◽  
1991 ◽  
Vol 113 (3) ◽  
pp. 985-994 ◽  
Author(s):  
A. Vaahtokari ◽  
S. Vainio ◽  
I. Thesleff
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Tooth Development ◽  
Brdu Incorporation ◽  
Oral Epithelium ◽  
Rna Expression ◽  
Tgf Beta ◽  
Growth Factor Beta ◽  
Dental Epithelium

We have studied the expression of transforming growth factor beta-1 (TGF-beta 1) RNA during mouse tooth development, using in situ hybridization and experimental tissue recombinations. Analysis of the serial sections revealed the appearance of local expression of TGF-beta 1 RNA in the dental epithelium at bud-staged teeth (13-day embryos). Just before transition to the cap stage, TGF-beta 1 RNA expression rapidly increased in the epithelial bud, and it also extended to the condensed dental mesenchyme. At cap stage (14- and 15-day embryos), there was an intense expression of TGF-beta 1 RNA in the morphologically active cervical loops of the dental epithelium. During early bell stage (16- and 17-day embryos), TGF-beta 1 RNA expression was detected in the inner enamel epithelium where it subsequently almost disappeared (18-day embryos). After birth TGF-beta 1 transcripts transiently appeared in these cells when they were differentiating into ameloblasts (1-day mice). The transcripts were lost from the ameloblasts when they became secretory (4-day mice), but the expression continued in ameloblasts in enamel-free areas. Transient expression of TGF-beta 1 RNA was also detected in epithelial stratum intermedium cells at the time of ameloblast differentiation. In the mesenchyme, TGF-beta 1 RNA was not detected during bell stage until it appeared in differentiated odontoblasts (18-day embryos). The secretory odontoblasts continued to express TGF-beta 1 RNA at all stages studied including the odontoblasts of incisor roots. Analysis of the distribution of bromodeoxyuridine (BrdU) incorporation indicated apparent correlations between TGF-beta 1 RNA expression and cell proliferation at the bud and cap stages but not at later stages of tooth development. Tissue recombination experiments of bud-staged (13-day embryos) dental and non-dental tissues showed that tooth epithelium, when cultured together with tooth mesenchyme, expressed TGF-beta 1 RNA. When the tooth epithelium was combined with non-dental jaw mesenchyme, TGF-beta 1 transcripts were not expressed. However, TGF-beta 1 RNA expression was seen in oral epithelium cultured with dental mesenchyme, while no expression of TGF-beta 1 transcripts was seen in the oral epithelium during normal development. Thus, TGF-beta 1 RNA expression seems to be regulated by epithelial-mesenchymal interactions.

Sonic hedgehog regulates growth and morphogenesis of the tooth

Development ◽  
2000 ◽  
Vol 127 (22) ◽  
pp. 4775-4785 ◽  
Author(s):  
H.R. Dassule ◽  
P. Lewis ◽  
M. Bei ◽  
R. Maas ◽  
A.P. McMahon
Keyword(s):  
Sonic Hedgehog ◽  
Tooth Development ◽  
Oral Epithelium ◽  
Signaling Proteins ◽  
Conditional Allele ◽  
Oral Ectoderm ◽  
In The Wild ◽  
Crown Formation ◽  
Dental Epithelium

During mammalian tooth development, the oral ectoderm and mesenchyme coordinate their growth and differentiation to give rise to organs with precise shapes, sizes and functions. The initial ingrowth of the dental epithelium and its associated dental mesenchyme gives rise to the tooth bud. Next, the epithelial component folds to give the tooth its shape. Coincident with this process, adjacent epithelial and mesenchymal cells differentiate into enamel-secreting ameloblasts and dentin-secreting odontoblasts, respectively. Growth, morphogenesis and differentiation of the epithelium and mesenchyme are coordinated by secreted signaling proteins. Sonic hedgehog (Shh) encodes a signaling peptide which is present in the oral epithelium prior to invagination and in the tooth epithelium throughout its development. We have addressed the role of Shh in the developing tooth in mouse by using a conditional allele to remove Shh activity shortly after ingrowth of the dental epithelium. Reduction and then loss of Shh function results in a cap stage tooth rudiment in which the morphology is severely disrupted. The overall size of the tooth is reduced and both the lingual epithelial invagination and the dental cord are absent. However, the enamel knot, a putative organizer of crown formation, is present and expresses Fgf4, Wnt10b, Bmp2 and Lef1, as in the wild type. At birth, the size and the shape of the teeth are severely affected and the polarity and organization of the ameloblast and odontoblast layers is disrupted. However, both dentin- and enamel-specific markers are expressed and a large amount of tooth-specific extracellular matrix is produced. This observation was confirmed by grafting studies in which tooth rudiments were cultured for several days under kidney capsules. Under these conditions, both enamel and dentin were deposited even though the enamel and dentin layers remained disorganized. These studies demonstrate that Shh regulates growth and determines the shape of the tooth. However, Shh signaling is not essential for differentiation of ameloblasts or odontoblasts.

scholarly journals An Irf6-Esrp1/2 regulatory axis controls midface morphogenesis in vertebrates

Development ◽  
2020 ◽  
Vol 147 (24) ◽  
pp. dev194498
Author(s):  
Shannon H. Carroll ◽  
Claudio Macias Trevino ◽  
Edward B. Li ◽  
Kenta Kawasaki ◽  
Nikita Myers ◽  
...  
Keyword(s):  
Cell Population ◽  
Genetic Interaction ◽  
Mouth Opening ◽  
Lineage Tracing ◽  
Oral Epithelium ◽  
Cranial Neural Crest Cells ◽  
Future Work ◽  
Double Homozygote ◽  
Complementary Analysis ◽  
Insight Into

ABSTRACTIrf6 and Esrp1 are important for palate development across vertebrates. In zebrafish, we found that irf6 regulates the expression of esrp1. We detailed overlapping Irf6 and Esrp1/2 expression in mouse orofacial epithelium. In zebrafish, irf6 and esrp1/2 share expression in periderm, frontonasal ectoderm and oral epithelium. Genetic disruption of irf6 and esrp1/2 in zebrafish resulted in cleft of the anterior neurocranium. The esrp1/2 mutant also developed cleft of the mouth opening. Lineage tracing of cranial neural crest cells revealed that the cleft resulted not from migration defect, but from impaired chondrogenesis. Analysis of aberrant cells within the cleft revealed expression of sox10, col1a1 and irf6, and these cells were adjacent to krt4+ and krt5+ cells. Breeding of mouse Irf6; Esrp1; Esrp2 compound mutants suggested genetic interaction, as the triple homozygote and the Irf6; Esrp1 double homozygote were not observed. Further, Irf6 heterozygosity reduced Esrp1/2 cleft severity. These studies highlight the complementary analysis of Irf6 and Esrp1/2 in mouse and zebrafish, and identify a unique aberrant cell population in zebrafish expressing sox10, col1a1 and irf6. Future work characterizing this cell population will yield additional insight into cleft pathogenesis.

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