The human enamel protein gene amelogenin is expressed from both the X and the Y chromosomes.
(41/161)
Amelogenins, a family of extracellular matrix proteins of the dental enamel, are transiently but abundantly expressed by ameloblasts during tooth development. Amelogenins seem to regulate the formation of crystallites during the secretory stage of enamel development, while they are specifically degraded during tooth-bud maturation. In this paper we report the characterization of the AMGX and AMGY genes on the short arms of the human X and Y chromosomes which encode the amelogenins. Our studies on the expression of the amelogenin genes in male developing tooth buds showed that both the AMGX and AMGY genes are transcriptionally active and encode potentially functional proteins. We have isolated genomic and cDNA clones from both the AMGX and AMGY loci and have studied the sequence organization of these two genes. Reverse transcriptase (RT)PCR amplification of the 5' portion of the amelogenin transcripts revealed several alternatively spliced products. The splicing pattern observed in the Y-derived mRNA varies from that of the X-derived mRNA. The promoter regions from both genes and the predicted amelogenin protein sequences are presented. This information will be useful for studying the molecular basis of X-linked amelogenesis imperfecta, for understanding the evolution and regulation of gene expression on the mammalian sex chromosomes, and for investigating the role of amelogenin genes during tooth development. (+info)
Expression survey of genes critical for tooth development in the human embryonic tooth germ.
(42/161)
In the developing murine tooth, the expression patterns of numerous regulatory genes have been examined and their roles have begun to be revealed. To unveil the molecular mechanisms that regulate human tooth morphogenesis, we examined the expression patterns of several regulatory genes, including BMP4, FGF8, MSX1, PAX9, PITX2, and SHOX2, and compared them with that found in mice. All of these genes are known to play critical roles in murine tooth development. Our results show that these genes exhibit basically similar expression patterns in the human tooth germ compared with that in the mouse. However, slightly different expression patterns were also observed for some of the genes at certain stages. For example, MSX1 expression was detected in the inner enamel epithelium in addition to the dental mesenchyme at the bell stage of the human tooth. Moreover, FGF8 expression remained in the dental epithelium at the cap stage, while PAX9 and SHOX2 expression was detected in both dental epithelium and mesenchyme of the human tooth germ. Our results indicate that, although slight differences exist in the gene expression patterns, the human and mouse teeth not only share considerable homology in odontogenesis but also use similar underlying molecular networks. (+info)
Diverse effects of c-src deficiency on molar tooth development and eruption in mice.
(43/161)
C-src deficiency is characterized by osteopetrosis due to impaired bone resorption by hypofunctional osteoclasts and the resultant failure of tooth eruption. In preliminary observations, we frequently encountered erupted molars in c-src deficient mice unlike in other osteopetrotic animals. Here we examine the effects of c-src deficiency on the development of molar teeth with an emphasis on the spatial relation of growing teeth with the surrounding bones. In c-src deficient mice, the magnitude of tooth impaction differed considerably among the types of molars; all maxillary 1st molars were totally impacted deep in the alveolar sockets, whereas most mandibular 1st molars fully erupted into oral cavity. Distribution of osteoclasts in the alveolar bone was identical among all types of molars, and electron microscopy revealed signs of bone resorbing activity in these osteoclasts despite the absence of a ruffled border. From early development, the alveolar space was much narrower in the upper molar tooth germs than in the lower ones in both wild type and homozygous animals, and particularly so in the upper 1st molars. Current observations thus indicate a significant contribution of "hypofunctional osteoclasts" in c-src deficient mice in molar tooth development except for the upper 1st molars, which appear to require highly functional osteoclasts to gain sufficient space for them to grow normally. Taken together, these findings on the seemingly tooth-type specific effects of c-src deficiency on the development and eruption of molar teeth in c-src deficient mice can be attributed to the given differential spatial relation of the respective tooth germs with the surrounding bones in the presence of hypofunctional osteoclasts. (+info)
Localization of Bmp-4, Shh and Wnt-5a transcripts during early mice tooth development by in situ hybridization.
(44/161)
A comparative nonisotopic in situ hybridization (ISH) analysis was carried out for the detection of Bmp-4, Shh and Wnt-5a transcripts during mice odontogenesis from initiation to cap stage. Bmp-4 was expressed early in the epithelium and then in the underlying mesenchyme. Shh expression was seen in the odontogenic epithelial lining thickening, being stronger in the enamel knot area, during the cap stage. Wnt-5a transcripts were expressed only in the mesenchyme during the initiation, bud and cap stages, with strong expression in the dental mesenchyme during the bud stage. The present results showed that Bmp-4, Shh and Wnt-5a are expressed since the very early stages of tooth development, and they suggest that the Wnt-5a gene is expressed in different cell populations than Bmp-4 and Shh. (+info)
Morphometric analysis of the developing murine molar tooth in vivo and in vitro.
(45/161)
A morphometric technique is described which has been used to measure morphogenesis and matrix synthesis of developing murine teeth in vivo and in vitro. The growth of bud and cap stage tooth germs in vitro was reduced considerably compared with in vivo. There was no growth of tooth germs explanted and cultured in vitro at the bell stage. The onset of dentine and enamel synthesis were however only slightly delayed in vitro compared with in vivo. The technique had been designed to be insensitive to orientation or artefactual folding of the cultured tissue. (+info)
Establishment, maintenance and modifications of the lower jaw dentition of wild Atlantic salmon (Salmo salar L.) throughout its life cycle.
(46/161)
In this paper we elucidate the pattern of initiation of the first teeth and the pattern of tooth replacement on the dentary of wild Atlantic salmon (Salmo salar L.), throughout nearly all stages of its life cycle, using serially sectioned heads and jaws, cleared and stained animals, and X-rays. The dentary teeth are set in one row. Tooth germs appear around hatching, first in odd positions, followed by even positions. From position 8 further backwards, teeth are added in adjacent positions. The first replacement teeth appear in animals of about 30 mm fork length. On the dentary of early life stages (alevins and fry), every position in the tooth row holds a functional (i.e. attached and erupted) tooth and a replacement tooth. The alternating pattern set up anteriorly in the dentary by the first-generation teeth changes in juveniles (parr) whereby teeth are in a similar functional (for the erupted teeth) or developmental stage (for the replacement teeth) every three positions. This pattern is also observed in marine animals during their marine life phase and in both sexes of adult animals prior to spawning (grilse and salmon), but every position now holds either a functional tooth or a mineralised replacement tooth. This is likely due to the fact that replacement tooth germs have to grow to a larger size before mineralisation starts. In the following spring, the dentary tooth pattern of animals that have survived spawning (kelts) is highly variable. The abundance of functional teeth in post-spawning animals nevertheless indicates that teeth are not lost over winter. We confirm the earlier reported lack of evidence for the existence of an edentulous life phase, preceding the appearance of so-called breeding teeth during upstream migration to the spawning grounds, and consider breeding teeth to be just another tooth generation in a regularly replacing dentition. This study shows how Atlantic salmon maintains a functional adaptive dentition throughout its complex life cycle. (+info)
Dental trigeminal nerve fiber growth and patterning are strictly integrated with tooth morphogenesis, but it is still unknown, how these two developmental processes are coordinated. Here we show that targeted inactivation of the dental epithelium expressed Fgfr2b results in cessation of the mouse mandibular first molar development at the degenerated cap stage and the failure of the trigeminal molar nerve to establish the lingual branch at E13.5 stage while the buccal branch develops properly. This axon patterning defect correlates to the histological absence of the mesenchymal dental follicle and adjacent Semaphorin3A-free dental follicle target field as well as appearance of ectopic Sema3A expression domain in the lingual side of the epithelial bud. Although the mesenchymal ligands for Fgfr2b, Fgf3 and -10 were present in the Fgfr2b(-/)(-) dental mesenchyme, mutant dental epithelium showed dramatically reduced proliferation and the lack of Fgf3. Tgfbeta1, which controls Sema3A was absent from the Fgfr2b(-/-) tooth germ, and Sema3A was specifically downregulated in the dental mesenchyme at the bud and cap stage. In addition, the epithelial primary enamel knot signaling center although being molecularly present neither was histologically detectable nor expressed Bmp4 and Fgf3 as well as Fgf4, which is essential for tooth morphogenesis and stimulates mesenchymal Fgf3 and Tgfbeta1. Fgf4 beads rescued Tgfbeta1 in the Fgfr2b(-/-) dental mesenchyme explants and Tgfbeta1 induced de novo Sema3A expression in the dental mesenchyme. Collectively these results demonstrate that epithelial Fgfr2b controls tooth morphogenesis and dental axon patterning, and suggests that Fgfr2b, by mediating local epithelial-mesenchymal interactions, integrates these two distinct developmental processes during odontogenesis. (+info)
Immunohistochemical localization of matrixmetalloproteinase-2 in human coronal dentin.
(48/161)
While it is known that matrixmetalloproteinase-2 (MMP-2) is present in dentin, its distribution and role in human dentin formation and pathology are not well understood. OBJECTIVE: To characterize the distribution of MMP-2 in human coronal dentin. METHODS: Immunohistochemistry was used to investigate the distribution of MMP-2 in coronal dentin. Freshly extracted human premolars and third molars (age range 12-30) were fixed with formaldehyde, demineralized with 10% EDTA (pH 7.4) and embedded in paraffin. Serial sections were made and subjected to immunohistochemical analysis using a specific monoclonal anti-MMP-2 antibody. Immunoreactivity was visualized with 3,3'-diaminobenzidine substrate and observed under light microscopy. ImageJ software was used to calculate the relative amount/distribution of MMP-2. RESULTS: The analysis revealed immunoreactivity for MMP-2 throughout human coronal dentin. However, intense immunoreactivities were identified in a 90-200 microm zone adjacent to the pre-dentin as well as a 9-10 microm wide zone adjacent to the dentinoenamel junction (DEJ). CONCLUSION: MMP-2 has a specific distribution in human coronal dentin indicating it's involvement in extracellular matrix organization in predentin and the establishment of the DEJ. (+info)