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Revitalization of a diastemal tooth primordium in Spry2 null mice results from increased proliferation and decreased apoptosis

Identifieur interne : 000153 ( France/Analysis ); précédent : 000152; suivant : 000154

Revitalization of a diastemal tooth primordium in Spry2 null mice results from increased proliferation and decreased apoptosis

Auteurs : Renata Peterkova [République tchèque, États-Unis] ; Svatava Churava [République tchèque] ; Herve Lesot [France, Royaume-Uni] ; Michaela Rothova [République tchèque] ; Jan Prochazka [République tchèque] ; Miroslav Peterka [République tchèque] ; Ophir D. Klein [États-Unis]

Source :

RBID : ISTEX:ECB51DFAF6AA56FBA9FD37985D1C2498853C8161

English descriptors

Abstract

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 rudimentary tooth primordia in mutant mice can help to lay the foundation for tooth regeneration by enhancing our knowledge of mechanisms that regulate tooth formation. J. Exp. Zool. (Mol. Dev. Evol.) 312B:292–308, 2009. © 2009 Wiley‐Liss, Inc.

Url:
DOI: 10.1002/jez.b.21266


Affiliations:


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ISTEX:ECB51DFAF6AA56FBA9FD37985D1C2498853C8161

Le document en format XML

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<title level="j" type="main">Journal of Experimental Zoology Part B: Molecular and Developmental Evolution</title>
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<term>Anterior</term>
<term>Anterior elevation</term>
<term>Anterior part</term>
<term>Apoptosis</term>
<term>Apoptotic</term>
<term>Apoptotic bodies</term>
<term>Apoptotic cells</term>
<term>Apoptotic elements</term>
<term>Biol</term>
<term>Biol peterkova</term>
<term>Cell death</term>
<term>Cheek region</term>
<term>Czech</term>
<term>Czech republic</term>
<term>Dental epithelium</term>
<term>Dentition</term>
<term>Diastema</term>
<term>Diastemal</term>
<term>Diastemal buds</term>
<term>Diastemal tooth primordium</term>
<term>Embryo</term>
<term>Embryonic</term>
<term>Enamel</term>
<term>Enamel knot</term>
<term>Enamel organ</term>
<term>Epithelial</term>
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<term>Evol</term>
<term>Fgf4</term>
<term>Frontal sections</term>
<term>Growth activators</term>
<term>Growth inhibitors</term>
<term>Histological</term>
<term>Histological sections</term>
<term>Incisor</term>
<term>Jernvall</term>
<term>Klein</term>
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<term>Lef1</term>
<term>Leica</term>
<term>Leica microsystems gmbh</term>
<term>Lesot</term>
<term>Lower molar</term>
<term>Mandible</term>
<term>Mesenchyme</term>
<term>Mitotic</term>
<term>Mitotic index</term>
<term>Molar</term>
<term>Molar epithelium</term>
<term>Molar region</term>
<term>More posteriorly</term>
<term>Morphogenesis</term>
<term>Mouse</term>
<term>Mutant</term>
<term>Mutant mice</term>
<term>Pathway</term>
<term>Peterka</term>
<term>Peterkova</term>
<term>Posterior diastemal</term>
<term>Posterior part</term>
<term>Premolar</term>
<term>Primordium</term>
<term>Quantitative evaluation</term>
<term>Regeneration</term>
<term>Revitalization</term>
<term>Ruch</term>
<term>Rudiment</term>
<term>Rudimentary diastemal</term>
<term>Rudiments</term>
<term>Sprouty</term>
<term>Spry2</term>
<term>Supernumerary</term>
<term>Supernumerary teeth</term>
<term>Supernumerary tooth</term>
<term>Supernumerary tooth primordium</term>
<term>Tabby</term>
<term>Thesleff</term>
<term>Tooth</term>
<term>Tooth development</term>
<term>Tooth primordia</term>
<term>Tooth regeneration</term>
<term>Tureckova</term>
<term>Viriot</term>
<term>Vonesch</term>
<term>Zool</term>
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<term>Anterior</term>
<term>Anterior elevation</term>
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<term>Apoptosis</term>
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<term>Apoptotic cells</term>
<term>Apoptotic elements</term>
<term>Biol</term>
<term>Biol peterkova</term>
<term>Cell death</term>
<term>Cheek region</term>
<term>Czech</term>
<term>Czech republic</term>
<term>Dental epithelium</term>
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<term>Diastema</term>
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<term>Diastemal buds</term>
<term>Diastemal tooth primordium</term>
<term>Embryo</term>
<term>Embryonic</term>
<term>Enamel</term>
<term>Enamel knot</term>
<term>Enamel organ</term>
<term>Epithelial</term>
<term>Epithelium</term>
<term>Evol</term>
<term>Fgf4</term>
<term>Frontal sections</term>
<term>Growth activators</term>
<term>Growth inhibitors</term>
<term>Histological</term>
<term>Histological sections</term>
<term>Incisor</term>
<term>Jernvall</term>
<term>Klein</term>
<term>Large diastemal buds</term>
<term>Lef1</term>
<term>Leica</term>
<term>Leica microsystems gmbh</term>
<term>Lesot</term>
<term>Lower molar</term>
<term>Mandible</term>
<term>Mesenchyme</term>
<term>Mitotic</term>
<term>Mitotic index</term>
<term>Molar</term>
<term>Molar epithelium</term>
<term>Molar region</term>
<term>More posteriorly</term>
<term>Morphogenesis</term>
<term>Mouse</term>
<term>Mutant</term>
<term>Mutant mice</term>
<term>Pathway</term>
<term>Peterka</term>
<term>Peterkova</term>
<term>Posterior diastemal</term>
<term>Posterior part</term>
<term>Premolar</term>
<term>Primordium</term>
<term>Quantitative evaluation</term>
<term>Regeneration</term>
<term>Revitalization</term>
<term>Ruch</term>
<term>Rudiment</term>
<term>Rudimentary diastemal</term>
<term>Rudiments</term>
<term>Sprouty</term>
<term>Spry2</term>
<term>Supernumerary</term>
<term>Supernumerary teeth</term>
<term>Supernumerary tooth</term>
<term>Supernumerary tooth primordium</term>
<term>Tabby</term>
<term>Thesleff</term>
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<term>Tooth primordia</term>
<term>Tooth regeneration</term>
<term>Tureckova</term>
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<div type="abstract" xml:lang="en">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 rudimentary tooth primordia in mutant mice can help to lay the foundation for tooth regeneration by enhancing our knowledge of mechanisms that regulate tooth formation. J. Exp. Zool. (Mol. Dev. Evol.) 312B:292–308, 2009. © 2009 Wiley‐Liss, Inc.</div>
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<name sortKey="Klein, Ophir D" sort="Klein, Ophir D" uniqKey="Klein O" first="Ophir D." last="Klein">Ophir D. Klein</name>
<name sortKey="Klein, Ophir D" sort="Klein, Ophir D" uniqKey="Klein O" first="Ophir D." last="Klein">Ophir D. Klein</name>
<name sortKey="Klein, Ophir D" sort="Klein, Ophir D" uniqKey="Klein O" first="Ophir D." last="Klein">Ophir D. Klein</name>
<name sortKey="Klein, Ophir D" sort="Klein, Ophir D" uniqKey="Klein O" first="Ophir D." last="Klein">Ophir D. Klein</name>
<name sortKey="Klein, Ophir D" sort="Klein, Ophir D" uniqKey="Klein O" first="Ophir D." last="Klein">Ophir D. Klein</name>
</country>
<country name="France">
<region name="Grand Est">
<name sortKey="Lesot, Herve" sort="Lesot, Herve" uniqKey="Lesot H" first="Herve" last="Lesot">Herve Lesot</name>
</region>
<name sortKey="Lesot, Herve" sort="Lesot, Herve" uniqKey="Lesot H" first="Herve" last="Lesot">Herve Lesot</name>
</country>
<country name="Royaume-Uni">
<noRegion>
<name sortKey="Lesot, Herve" sort="Lesot, Herve" uniqKey="Lesot H" first="Herve" last="Lesot">Herve Lesot</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>

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