The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Lu Li - One of the best experts on this subject based on the ideXlab platform.
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exogenous fibroblast growth factor 8 rescues development of mouse Diastemal vestigial tooth ex vivo
Developmental Dynamics, 2011Co-Authors: Guohua Yuan, Yanding Zhang, Lu Li, Lu Zhang, Yiping Chen, Zhi ChenAbstract:Regression of vestigial tooth buds results in the formation of the toothless Diastema, a unique feature of the mouse dentition. Revitalization of the Diastemal vestigial tooth bud provides an excellent model for studying tooth regeneration and replacement. It was shown previously that suppression of FGF signaling in the Diastema is a causative of vestigial tooth bud regression. In this study, we report that application of exogenous FGF8 to the mouse embryonic Diastemal region rescues Diastemal tooth development. However, this rescue of Diastemal tooth development occurs only in isolated Diastemal region, but not in mandibular quadrant containing incisor and molar germs. FGF8 promotes cell proliferation and inhibits apoptosis in Diastemal tooth epithelium, and revitalizes tooth developmental program, evidenced by the expression of genes critical for normal tooth development. Our results support the idea that the adjacent tooth germs contribute to the suppression of Diastemal vestigial tooth buds via multiple signals.
Jukka Jernvall - One of the best experts on this subject based on the ideXlab platform.
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sprouty genes control Diastema tooth development via bidirectional antagonism of epithelial mesenchymal fgf signaling
Developmental Cell, 2006Co-Authors: Ophir D Klein, Renata Peterková, George Minowada, Aapo T Kangas, H Lesot, M Peterka, Jukka Jernvall, Gail R MartinAbstract:Unlike humans, who have a continuous row of teeth, mice have only molars and incisors separated by a toothless region called a Diastema. Although tooth buds form in the embryonic Diastema, they regress and do not develop into teeth. Here, we identify members of the Sprouty (Spry) family, which encode negative feedback regulators of fibroblast growth factor (FGF) and other receptor tyrosine kinase signaling, as genes that repress Diastema tooth development. We show that different Sprouty genes are deployed in different tissue compartments—Spry2 in epithelium and Spry4 in mesenchyme—to prevent Diastema tooth formation. We provide genetic evidence that they function to ensure that Diastema tooth buds are refractory to signaling via FGF ligands that are present in the region and thus prevent these buds from engaging in the FGF-mediated bidirectional signaling between epithelium and mesenchyme that normally sustains tooth development.
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gene expression patterns associated with suppression of odontogenesis in mouse and vole Diastema regions
Development Genes and Evolution, 1999Co-Authors: Soile Keranen, Paivi Kettunen, Thomas Aberg, Irma Thesleff, Jukka JernvallAbstract:Rodents have a toothless Diastema region between the incisor and molar teeth which may contain rudimentary tooth germs. We found in upper Diastema region of the mouse (Musmusculus) three small tooth germs which developed into early bud stage before their apoptotic removal, while the sibling vole (Microtusrossiaemeridionalis) had only a single but larger tooth germ in this region, and this developed into late bud stage before regressing apoptotically. To analyze the genetic mechanisms of the developmental arrest of the rudimentary tooth germs we compared the expression patterns of several developmental regulatory genes (Bmp2, Bmp4, Fgf4, Fgf8, Lef1, Msx1, Msx2, p21, Pitx2, Pax9 and Shh) between molars and Diastema buds of mice and voles. In Diastema tooth buds the expression of all the genes differed from that of molars. The gene expression patterns suggest that the odontogenic program consists of partially independent signaling cascades which define the exact location of the tooth germ, initiate epithelial budding, and transfer the odontogenic potential from the epithelium to the underlying mesenchyma. Although the Diastema regions of the two species differed, in both species the earliest difference that we found was weaker expression of mesenchymal Pax9 in the Diastema region than in molar and incisor regions at the dental lamina stage. However, based on earlier tissue recombination experiments it is conceivable that the developmental arrest is determined by the early oral epithelium.
Renata Peterková - One of the best experts on this subject based on the ideXlab platform.
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revitalization of a Diastemal tooth primordium in spry2 null mice results from increased proliferation and decreased apoptosis
Journal of Experimental Zoology, 2009Co-Authors: Renata Peterková, Hervé Lesot, Svatava Churava, Michaela Rothova, Jan Prochazka, Miroslav PeterkaAbstract:An understanding of the factors that promote or inhibit tooth development is essential for designing biological tooth replacements. The embryonic mouse dentition provides an ideal system for studying such factors because it consists of two types of tooth primordia. One type of primordium will go on to form a functional tooth, whereas the other initiates development but arrests at or before the bud stage. This developmental arrest contributes to the formation of the toothless mouse Diastema. It is accompanied by the apoptosis of the rudimentary Diastemal buds, which presumably results from the insufficient activity of anti-apoptotic signals such as fibroblast growth factors (FGFs). We have previously shown that the arrest of a rudimentary tooth bud can be rescued by inactivating Spry2, an antagonist of FGF signaling. Here, we studied the role of the epithelial cell death and proliferation in this process by comparing the development of a rudimentary Diastemal tooth bud (R2) and the first molar in the mandibles of Spry2 / and wild-type (WT) embryos using histological sections, image analysis and 3D reconstructions. In the WT R2 at embryonic day 13.5, significantly increased apoptosis and decreased proliferation were found compared with the first molar. In contrast, increased levels of FGF signaling in Spry2 / embryos led to significantly decreased apoptosis and increased proliferation in the R2 bud. Consequently, the R2 was involved in the formation of a supernumerary tooth primordium. Studies of the revitalization of
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primary cilia regulate shh activity in the control of molar tooth number
Development, 2009Co-Authors: Atsushi Ohazama, Renata Peterková, Courtney J Haycraft, Maisa Seppala, James Blackburn, Sarah Ghafoor, Martyn T Cobourne, David C Martinelli, Chenming Fan, Hervé LesotAbstract:Primary cilia mediate Hh signalling and mutations in their protein components affect Hh activity. We show that in mice mutant for a cilia intraflagellar transport (IFT) protein, IFT88/polaris, Shh activity is increased in the toothless Diastema mesenchyme of the embryonic jaw primordia. This results in the formation of ectopic teeth in the Diastema, mesial to the first molars. This phenotype is specific to loss of polaris activity in the mesenchyme since loss of Polaris in the epithelium has no detrimental affect on tooth development. To further confirm that upregulation of Shh activity is responsible for the ectopic tooth formation, we analysed mice mutant for Gas1, a Shh protein antagonist in Diastema mesenchyme. Gas1 mutants also had ectopic Diastema teeth and accompanying increased Shh activity. In this context, therefore, primary cilia exert a specific negative regulatory effect on Shh activity that functions to repress tooth formation and thus determine tooth number. Strikingly, the ectopic teeth adopt a size and shape characteristic of premolars, a tooth type that was lost in mice around 50-100 million years ago.
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sprouty genes control Diastema tooth development via bidirectional antagonism of epithelial mesenchymal fgf signaling
Developmental Cell, 2006Co-Authors: Ophir D Klein, Renata Peterková, George Minowada, Aapo T Kangas, H Lesot, M Peterka, Jukka Jernvall, Gail R MartinAbstract:Unlike humans, who have a continuous row of teeth, mice have only molars and incisors separated by a toothless region called a Diastema. Although tooth buds form in the embryonic Diastema, they regress and do not develop into teeth. Here, we identify members of the Sprouty (Spry) family, which encode negative feedback regulators of fibroblast growth factor (FGF) and other receptor tyrosine kinase signaling, as genes that repress Diastema tooth development. We show that different Sprouty genes are deployed in different tissue compartments—Spry2 in epithelium and Spry4 in mesenchyme—to prevent Diastema tooth formation. We provide genetic evidence that they function to ensure that Diastema tooth buds are refractory to signaling via FGF ligands that are present in the region and thus prevent these buds from engaging in the FGF-mediated bidirectional signaling between epithelium and mesenchyme that normally sustains tooth development.
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Origin and developmental fate of vestigial tooth primordia in the upper Diastema of the field vole (Microtus agrestis, Rodentia).
Archives of Oral Biology, 2005Co-Authors: Kirsti Witter, Ivan Míšek, Hervé Lesot, Miroslav Peterka, Jean-luc Vonesch, Renata PeterkováAbstract:OBJECTIVE: Odontogenesis in voles is a convenient model to test hypotheses on tooth development generated from investigations in the mouse. Similar to other rodents, the functional dentition of the vole includes a toothless Diastema. At its mesial end, a vestigial tooth bud has been found in the upper jaw of vole embryos. The aim of this study was to analyse the developmental dynamics of vestigial tooth structures in the upper Diastema of the field vole and to compare it with the situation in the mouse. DESIGN: The development of odontogenic structures in the upper Diastema of the field vole was investigated using serial histological sections and three-dimensional (3D) computer-aided reconstruction. RESULTS: A transient continuous dental lamina in the upper Diastema of the field vole extended mesially to the first molar primordium, but was not continuous with the dental lamina in the incisor region. At its mesial limit, a large vestigial tooth primordium was regularly present. A further distinct vestigial bud was located mesially to the first molar primordium. The segmentation of the dental lamina suggested a potential to give rise to further vestiges in the upper Diastema of the vole. CONCLUSIONS: In the prospective Diastema of the vole exists as in the mouse a continuous dental lamina. Beside the prominent vestigial tooth bud in the mesial Diastema, a further large bud was transiently located in front of the molars. The incorporation of dental epithelium into the first upper molar (M(1)) primordium in the vole differs from that in the mouse.
Zhi Chen - One of the best experts on this subject based on the ideXlab platform.
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exogenous fibroblast growth factor 8 rescues development of mouse Diastemal vestigial tooth ex vivo
Developmental Dynamics, 2011Co-Authors: Guohua Yuan, Yanding Zhang, Lu Li, Lu Zhang, Yiping Chen, Zhi ChenAbstract:Regression of vestigial tooth buds results in the formation of the toothless Diastema, a unique feature of the mouse dentition. Revitalization of the Diastemal vestigial tooth bud provides an excellent model for studying tooth regeneration and replacement. It was shown previously that suppression of FGF signaling in the Diastema is a causative of vestigial tooth bud regression. In this study, we report that application of exogenous FGF8 to the mouse embryonic Diastemal region rescues Diastemal tooth development. However, this rescue of Diastemal tooth development occurs only in isolated Diastemal region, but not in mandibular quadrant containing incisor and molar germs. FGF8 promotes cell proliferation and inhibits apoptosis in Diastemal tooth epithelium, and revitalizes tooth developmental program, evidenced by the expression of genes critical for normal tooth development. Our results support the idea that the adjacent tooth germs contribute to the suppression of Diastemal vestigial tooth buds via multiple signals.
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mesenchyme is responsible for tooth suppression in the mouse lower Diastema
Journal of Dental Research, 2008Co-Authors: Guohua Yuan, Li Zhang, Yanding Zhang, Mingwen Fan, Zhuan Bian, Zhi ChenAbstract:Between the incisor and molars in each dental quadrant, mice have a toothless gap (Diastema) that may contain vestigial tooth primordia. It is still not clear whether suppression of odontogenesis in the mouse lower Diastema can be attributed to epithelium, mesenchyme, or both. Therefore, using recombination experiments with mouse tissues from E11.5 and E13.5 stages, we investigated whether the epithelium or mesenchyme is responsible for the suppression of odontogenesis. Five groups of recombinants were established and cultured under mouse kidney capsules. The results demonstrated that at E11.5, the lower Diastemal epithelium and mesenchyme possessed odontogenic potential and competence, respectively; at E13.5, both the lower Diastemal epithelium and mesenchyme had odontogenic competence, while the lower Diastemal mesenchyme did not possess odontogenic potential. On the basis of comparison of the odontogenic capabilities between the lower Diastemal and molar tooth primordia, we conclude that mesenchyme is responsible for tooth regression in the mouse lower Diastema.
Yiping Chen - One of the best experts on this subject based on the ideXlab platform.
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exogenous fibroblast growth factor 8 rescues development of mouse Diastemal vestigial tooth ex vivo
Developmental Dynamics, 2011Co-Authors: Guohua Yuan, Yanding Zhang, Lu Li, Lu Zhang, Yiping Chen, Zhi ChenAbstract:Regression of vestigial tooth buds results in the formation of the toothless Diastema, a unique feature of the mouse dentition. Revitalization of the Diastemal vestigial tooth bud provides an excellent model for studying tooth regeneration and replacement. It was shown previously that suppression of FGF signaling in the Diastema is a causative of vestigial tooth bud regression. In this study, we report that application of exogenous FGF8 to the mouse embryonic Diastemal region rescues Diastemal tooth development. However, this rescue of Diastemal tooth development occurs only in isolated Diastemal region, but not in mandibular quadrant containing incisor and molar germs. FGF8 promotes cell proliferation and inhibits apoptosis in Diastemal tooth epithelium, and revitalizes tooth developmental program, evidenced by the expression of genes critical for normal tooth development. Our results support the idea that the adjacent tooth germs contribute to the suppression of Diastemal vestigial tooth buds via multiple signals.