Revitalization of a diastemal tooth primordium in Spry2 null mice results from increased proliferation and decreased apoptosis
Identifieur interne : 007542 ( Istex/Corpus ); précédent : 007541; suivant : 007543Revitalization of a diastemal tooth primordium in Spry2 null mice results from increased proliferation and decreased apoptosis
Auteurs : Renata Peterkova ; Svatava Churava ; Herve Lesot ; Michaela Rothova ; Jan Prochazka ; Miroslav Peterka ; Ophir D. KleinSource :
- Journal of Experimental Zoology Part B: Molecular and Developmental Evolution [ 1552-5007 ] ; 2009-06-15.
English descriptors
- KwdEn :
- Anterior, Anterior elevation, Anterior part, Apoptosis, Apoptotic, Apoptotic bodies, Apoptotic cells, Apoptotic elements, Biol, Biol peterkova, Cell death, Cheek region, Czech, Czech republic, Dental epithelium, Dentition, Diastema, Diastemal, Diastemal buds, Diastemal tooth primordium, Embryo, Embryonic, Enamel, Enamel knot, Enamel organ, Epithelial, Epithelium, Evol, Fgf4, Frontal sections, Growth activators, Growth inhibitors, Histological, Histological sections, Incisor, Jernvall, Klein, Large diastemal buds, Lef1, Leica, Leica microsystems gmbh, Lesot, Lower molar, Mandible, Mesenchyme, Mitotic, Mitotic index, Molar, Molar epithelium, Molar region, More posteriorly, Morphogenesis, Mouse, Mutant, Mutant mice, Pathway, Peterka, Peterkova, Posterior diastemal, Posterior part, Premolar, Primordium, Quantitative evaluation, Regeneration, Revitalization, Ruch, Rudiment, Rudimentary diastemal, Rudiments, Sprouty, Spry2, Supernumerary, Supernumerary teeth, Supernumerary tooth, Supernumerary tooth primordium, Tabby, Thesleff, Tooth, Tooth development, Tooth primordia, Tooth regeneration, Tureckova, Viriot, Vonesch, Zool.
- Teeft :
- Anterior, Anterior elevation, Anterior part, Apoptosis, Apoptotic, Apoptotic bodies, Apoptotic cells, Apoptotic elements, Biol, Biol peterkova, Cell death, Cheek region, Czech, Czech republic, Dental epithelium, Dentition, Diastema, Diastemal, Diastemal buds, Diastemal tooth primordium, Embryo, Embryonic, Enamel, Enamel knot, Enamel organ, Epithelial, Epithelium, Evol, Fgf4, Frontal sections, Growth activators, Growth inhibitors, Histological, Histological sections, Incisor, Jernvall, Klein, Large diastemal buds, Lef1, Leica, Leica microsystems gmbh, Lesot, Lower molar, Mandible, Mesenchyme, Mitotic, Mitotic index, Molar, Molar epithelium, Molar region, More posteriorly, Morphogenesis, Mouse, Mutant, Mutant mice, Pathway, Peterka, Peterkova, Posterior diastemal, Posterior part, Premolar, Primordium, Quantitative evaluation, Regeneration, Revitalization, Ruch, Rudiment, Rudimentary diastemal, Rudiments, Sprouty, Spry2, Supernumerary, Supernumerary teeth, Supernumerary tooth, Supernumerary tooth primordium, Tabby, Thesleff, Tooth, Tooth development, Tooth primordia, Tooth regeneration, Tureckova, Viriot, Vonesch, Zool.
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
Links to Exploration step
ISTEX:ECB51DFAF6AA56FBA9FD37985D1C2498853C8161Le document en format XML
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Klein</name><affiliation><mods:affiliation>Department of Orofacial Sciences, University of California, San Francisco, California</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Pediatrics, University of California, San Francisco, California</mods:affiliation></affiliation><affiliation><mods:affiliation>Institutes of Human Genetics and Regeneration Medicine, University of California, San Francisco, California</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: Ophir.Klein@ucsf.edu</mods:affiliation></affiliation><affiliation><mods:affiliation>Renata Peterkova, Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, v.v.i., Videnska 1083, 14220 Prague, Czech Republic===Ophir D. 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Klein, Departments of Orofacial Sciences and Pediatrics, University of California, San Francisco, CA 94143‐0442 USA===</mods:affiliation></affiliation></author><author><name sortKey="Churava, Svatava" sort="Churava, Svatava" uniqKey="Churava S" first="Svatava" last="Churava">Svatava Churava</name><affiliation><mods:affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Anthropology, Faculty of Science, Charles University, Prague, Czech Republic</mods:affiliation></affiliation></author><author><name sortKey="Lesot, Herve" sort="Lesot, Herve" uniqKey="Lesot H" first="Herve" last="Lesot">Herve Lesot</name><affiliation><mods:affiliation>INSERM U595, Faculté de Médecine, Université Louis Pasteur, Strasbourg, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Faculté de Chirurgie Dentaire, Université Louis Pasteur, Strasbourg, France</mods:affiliation></affiliation><affiliation><mods:affiliation>International Collaborating Centre in Oro‐Facial Genetics and Development, University of Liverpool, Liverpool, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Rothova, Michaela" sort="Rothova, Michaela" uniqKey="Rothova M" first="Michaela" last="Rothova">Michaela Rothova</name><affiliation><mods:affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Developmental Biology, Faculty of Science, Charles University, Prague, Czech Republic</mods:affiliation></affiliation></author><author><name sortKey="Prochazka, Jan" sort="Prochazka, Jan" uniqKey="Prochazka J" first="Jan" last="Prochazka">Jan Prochazka</name><affiliation><mods:affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Developmental Biology, Faculty of Science, Charles University, Prague, Czech Republic</mods:affiliation></affiliation></author><author><name sortKey="Peterka, Miroslav" sort="Peterka, Miroslav" uniqKey="Peterka M" first="Miroslav" last="Peterka">Miroslav Peterka</name><affiliation><mods:affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Anthropology, Faculty of Science, Charles University, Prague, Czech Republic</mods:affiliation></affiliation></author><author><name sortKey="Klein, Ophir D" sort="Klein, Ophir D" uniqKey="Klein O" first="Ophir D." last="Klein">Ophir D. Klein</name><affiliation><mods:affiliation>Department of Orofacial Sciences, University of California, San Francisco, California</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Pediatrics, University of California, San Francisco, California</mods:affiliation></affiliation><affiliation><mods:affiliation>Institutes of Human Genetics and Regeneration Medicine, University of California, San Francisco, California</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: Ophir.Klein@ucsf.edu</mods:affiliation></affiliation><affiliation><mods:affiliation>Renata Peterkova, Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, v.v.i., Videnska 1083, 14220 Prague, Czech Republic===Ophir D. Klein, Departments of Orofacial Sciences and Pediatrics, University of California, San Francisco, CA 94143‐0442 USA===</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Experimental Zoology Part B: Molecular and Developmental Evolution</title><title level="j" type="sub">Tooth Development in Evolution and Disease, Part 1</title><title level="j" type="alt">JOURNAL OF EXPERIMENTAL ZOOLOGY PART B: MOLECULAR AND DEVELOPMENTAL EVOLUTION</title><idno type="ISSN">1552-5007</idno><idno type="eISSN">1552-5015</idno><imprint><biblScope unit="vol">312B</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="292">292</biblScope><biblScope unit="page" to="308">308</biblScope><biblScope unit="page-count">17</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-06-15">2009-06-15</date></imprint><idno type="ISSN">1552-5007</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1552-5007</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><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><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><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></keywords><keywords scheme="Teeft" xml:lang="en"><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><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><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></keywords></textClass></profileDesc></teiHeader><front><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></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>epithelium</json:string><json:string>peterkova</json:string><json:string>apoptosis</json:string><json:string>diastemal</json:string><json:string>dental epithelium</json:string><json:string>spry2</json:string><json:string>mutant</json:string><json:string>primordium</json:string><json:string>supernumerary</json:string><json:string>molar</json:string><json:string>lesot</json:string><json:string>apoptotic</json:string><json:string>biol</json:string><json:string>supernumerary tooth</json:string><json:string>viriot</json:string><json:string>anterior part</json:string><json:string>peterka</json:string><json:string>mandible</json:string><json:string>embryo</json:string><json:string>morphogenesis</json:string><json:string>evol</json:string><json:string>zool</json:string><json:string>epithelial</json:string><json:string>mitotic</json:string><json:string>enamel</json:string><json:string>diastema</json:string><json:string>dentition</json:string><json:string>molar epithelium</json:string><json:string>premolar</json:string><json:string>enamel knot</json:string><json:string>revitalization</json:string><json:string>jernvall</json:string><json:string>vonesch</json:string><json:string>rudiment</json:string><json:string>frontal sections</json:string><json:string>tooth development</json:string><json:string>mesenchyme</json:string><json:string>ruch</json:string><json:string>thesleff</json:string><json:string>incisor</json:string><json:string>leica</json:string><json:string>klein</json:string><json:string>mitotic index</json:string><json:string>molar region</json:string><json:string>rudiments</json:string><json:string>tabby</json:string><json:string>czech</json:string><json:string>cheek region</json:string><json:string>pathway</json:string><json:string>sprouty</json:string><json:string>fgf4</json:string><json:string>diastemal tooth primordium</json:string><json:string>apoptotic cells</json:string><json:string>czech republic</json:string><json:string>supernumerary tooth primordium</json:string><json:string>posterior part</json:string><json:string>quantitative evaluation</json:string><json:string>tureckova</json:string><json:string>lef1</json:string><json:string>histological</json:string><json:string>mouse</json:string><json:string>leica microsystems gmbh</json:string><json:string>tooth primordia</json:string><json:string>growth inhibitors</json:string><json:string>lower molar</json:string><json:string>posterior diastemal</json:string><json:string>mutant mice</json:string><json:string>histological sections</json:string><json:string>embryonic</json:string><json:string>anterior</json:string><json:string>large diastemal buds</json:string><json:string>rudimentary diastemal</json:string><json:string>supernumerary teeth</json:string><json:string>apoptotic elements</json:string><json:string>diastemal buds</json:string><json:string>enamel organ</json:string><json:string>apoptotic bodies</json:string><json:string>growth activators</json:string><json:string>anterior elevation</json:string><json:string>tooth regeneration</json:string><json:string>more posteriorly</json:string><json:string>cell death</json:string><json:string>biol peterkova</json:string><json:string>regeneration</json:string><json:string>tooth</json:string></teeft></keywords><author><json:item><name>Renata Peterkova</name><affiliations><json:string>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</json:string><json:string>E-mail: repete@biomed.cas.cz</json:string><json:string>Renata Peterkova, Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, v.v.i., Videnska 1083, 14220 Prague, Czech Republic===Ophir D. Klein, Departments of Orofacial Sciences and Pediatrics, University of California, San Francisco, CA 94143‐0442 USA===</json:string></affiliations></json:item><json:item><name>Svatava Churava</name><affiliations><json:string>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</json:string><json:string>Department of Anthropology, Faculty of Science, Charles University, Prague, Czech Republic</json:string></affiliations></json:item><json:item><name>Herve Lesot</name><affiliations><json:string>INSERM U595, Faculté de Médecine, Université Louis Pasteur, Strasbourg, France</json:string><json:string>Faculté de Chirurgie Dentaire, Université Louis Pasteur, Strasbourg, France</json:string><json:string>International Collaborating Centre in Oro‐Facial Genetics and Development, University of Liverpool, Liverpool, United Kingdom</json:string></affiliations></json:item><json:item><name>Michaela Rothova</name><affiliations><json:string>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</json:string><json:string>Department of Developmental Biology, Faculty of Science, Charles University, Prague, Czech Republic</json:string></affiliations></json:item><json:item><name>Jan Prochazka</name><affiliations><json:string>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</json:string><json:string>Department of Developmental Biology, Faculty of Science, Charles University, Prague, Czech Republic</json:string></affiliations></json:item><json:item><name>Miroslav Peterka</name><affiliations><json:string>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</json:string><json:string>Department of Anthropology, Faculty of Science, Charles University, Prague, Czech Republic</json:string></affiliations></json:item><json:item><name>Ophir D. Klein</name><affiliations><json:string>Department of Orofacial Sciences, University of California, San Francisco, California</json:string><json:string>Department of Pediatrics, University of California, San Francisco, California</json:string><json:string>Institutes of Human Genetics and Regeneration Medicine, University of California, San Francisco, California</json:string><json:string>E-mail: Ophir.Klein@ucsf.edu</json:string><json:string>Renata Peterkova, Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, v.v.i., Videnska 1083, 14220 Prague, Czech Republic===Ophir D. Klein, Departments of Orofacial Sciences and Pediatrics, University of California, San Francisco, CA 94143‐0442 USA===</json:string></affiliations></json:item></author><articleId><json:string>JEZ21266</json:string></articleId><arkIstex>ark:/67375/WNG-LSZL3TWZ-P</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><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.</abstract><qualityIndicators><score>10</score><pdfWordCount>8937</pdfWordCount><pdfCharCount>53547</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>17</pdfPageCount><pdfPageSize>595.276 x 793.701 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>271</abstractWordCount><abstractCharCount>1788</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Revitalization of a diastemal tooth primordium in Spry2 null mice results from increased proliferation and decreased apoptosis</title><pmid><json:string>19127536</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Journal of Experimental Zoology Part B: Molecular and Developmental Evolution</title><language><json:string>unknown</json:string></language><doi><json:string>10.1002/(ISSN)1552-5015</json:string></doi><issn><json:string>1552-5007</json:string></issn><eissn><json:string>1552-5015</json:string></eissn><publisherId><json:string>JEZ</json:string></publisherId><volume>312B</volume><issue>4</issue><pages><first>292</first><last>308</last><total>17</total></pages><genre><json:string>journal</json:string></genre><author><json:item><name>Thimios Mitsiadis</name></json:item><json:item><name>Herve Lesot</name></json:item><json:item><name>Moya Smith</name></json:item></author><subject><json:item><value>Research Article</value></json:item></subject></host><namedEntities><unitex><date><json:string>2009</json:string></date><geogName></geogName><orgName><json:string>Histochem</json:string><json:string>Department of Pediatrics, University of California, San Francisco, California</json:string><json:string>Wiley-Liss, Inc.</json:string><json:string>University of California, San Francisco</json:string><json:string>University of Liverpool</json:string><json:string>Department of Orofacial Sciences, University of California, San Francisco, California</json:string><json:string>Department of Anthropology, Faculty of Science, Charles University, Prague, Czech Republic</json:string><json:string>LISS, INC.</json:string><json:string>Department of Developmental Biology, Faculty of Science, Charles University, Prague, Czech Republic</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Dev Cell</json:string><json:string>Zdenka Lisa</json:string><json:string>Iva Koppova</json:string><json:string>J. 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Fluck</json:string><json:string>Dev Evol</json:string><json:string>Dev Biol</json:string></persName><placeName><json:string>Switzerland</json:string><json:string>Germany</json:string><json:string>Strasbourg</json:string><json:string>Liverpool</json:string><json:string>Basel</json:string><json:string>United Kingdom</json:string><json:string>Murcia</json:string><json:string>Wetzlar</json:string><json:string>France</json:string></placeName><ref_url><json:string>http://rsb.info.nih.gov/ij/</json:string></ref_url><ref_bibl><json:string>Peterkova et al., 2006</json:string><json:string>Hu et al., 2006</json:string><json:string>Coin et al.</json:string><json:string>Nadiri et al., 2004</json:string><json:string>Boran et al., 2005</json:string><json:string>Zhang et al., 2003</json:string><json:string>Duailibi et al., 2006</json:string><json:string>Nie et al., 2006</json:string><json:string>Peterkova et al., 2000</json:string><json:string>Celli et al.</json:string><json:string>Peterkova et al., 2002a</json:string><json:string>Elomaa et al., 2001</json:string><json:string>Peterkova et al., 2005, 2006</json:string><json:string>Peterkova et al., 2005</json:string><json:string>Tureckova et al.</json:string><json:string>Coin et al., 2000b</json:string><json:string>Viriot et al.</json:string><json:string>Viriot et al., 2000</json:string><json:string>Kristenova et al., 2002</json:string><json:string>Peterkova et al., 2002b, 2005</json:string><json:string>Shim et al., 2005</json:string><json:string>Tucker et al., 2004</json:string><json:string>Lesot et al.</json:string><json:string>Weiss et al.</json:string><json:string>Setkova et al., 2007</json:string><json:string>Jernvall and Thesleff, 2000</json:string><json:string>Laurikkala et al., 2001</json:string><json:string>Yen and Sharpe, 2006</json:string><json:string>Jernvall et al.</json:string><json:string>Obara and Lesot, 2007</json:string><json:string>Peterkova et al., 2003</json:string><json:string>Peterkova et al., 2000, 2003</json:string><json:string>Zhang et al., 2000</json:string><json:string>Kangas et al., 2004</json:string><json:string>Peterkova et al., 2000, 2002a</json:string><json:string>Peterkova et al.</json:string><json:string>MacKenzie et al.</json:string><json:string>Kavanagh et al., 2007</json:string><json:string>Vaahtokari et al.</json:string><json:string>D’Souza and Klein, 2007</json:string><json:string>Hovorakova et al., 2005</json:string><json:string>Kratochwil et al., 2002</json:string><json:string>Klein et al., 2006</json:string><json:string>Peterka et al., 2002</json:string><json:string>Matalova et al., 2006</json:string><json:string>Sasaki et al., 2005</json:string><json:string>Viriot et al., 2002</json:string><json:string>Pummila et al., 2007</json:string><json:string>Klein et al., 2006, 2008</json:string><json:string>Kassai et al., 2005</json:string><json:string>Peterkova et al., 2002b</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-LSZL3TWZ-P</json:string></ark><categories><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences biologiques fondamentales et appliquees. psychologie</json:string></inist></categories><publicationDate>2009</publicationDate><copyrightDate>2009</copyrightDate><doi><json:string>10.1002/jez.b.21266</json:string></doi><id>ECB51DFAF6AA56FBA9FD37985D1C2498853C8161</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/ECB51DFAF6AA56FBA9FD37985D1C2498853C8161/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/ECB51DFAF6AA56FBA9FD37985D1C2498853C8161/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/ECB51DFAF6AA56FBA9FD37985D1C2498853C8161/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Revitalization of a diastemal tooth primordium in <hi rend="italic">Spry2</hi> null mice results from increased proliferation and decreased apoptosis</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><licence>Copyright © 2009 Wiley‐Liss, Inc., A Wiley Company</licence></availability><date type="published" when="2009-06-15"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main" xml:lang="en">Revitalization of a diastemal tooth primordium in <hi rend="italic">Spry2</hi> null mice results from increased proliferation and decreased apoptosis</title><title level="a" type="short" xml:lang="en">REVITALIZATION OF DIASTEMAL TOOTH PRIMORDIUM</title><author xml:id="author-0000" role="corresp"><persName><forename type="first">Renata</forename><surname>Peterkova</surname></persName><email>repete@biomed.cas.cz</email><affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic<address><country key="CZ"></country></address></affiliation><affiliation>Renata Peterkova, Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, v.v.i., Videnska 1083, 14220 Prague, Czech Republic=== Ophir D. Klein, Departments of Orofacial Sciences and Pediatrics, University of California, San Francisco, CA 94143‐0442 USA===</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Svatava</forename><surname>Churava</surname></persName><affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic<address><country key="CZ"></country></address></affiliation><affiliation>Department of Anthropology, Faculty of Science, Charles University, Prague, Czech Republic<address><country key="CZ"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Herve</forename><surname>Lesot</surname></persName><affiliation>INSERM U595, Faculté de Médecine, Université Louis Pasteur, Strasbourg, France<address><country key="FR"></country></address></affiliation><affiliation>Faculté de Chirurgie Dentaire, Université Louis Pasteur, Strasbourg, France<address><country key="FR"></country></address></affiliation><affiliation>International Collaborating Centre in Oro‐Facial Genetics and Development, University of Liverpool, Liverpool, United Kingdom<address><country key="GB"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Michaela</forename><surname>Rothova</surname></persName><affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic<address><country key="CZ"></country></address></affiliation><affiliation>Department of Developmental Biology, Faculty of Science, Charles University, Prague, Czech Republic<address><country key="CZ"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Jan</forename><surname>Prochazka</surname></persName><affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic<address><country key="CZ"></country></address></affiliation><affiliation>Department of Developmental Biology, Faculty of Science, Charles University, Prague, Czech Republic<address><country key="CZ"></country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Miroslav</forename><surname>Peterka</surname></persName><affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic<address><country key="CZ"></country></address></affiliation><affiliation>Department of Anthropology, Faculty of Science, Charles University, Prague, Czech Republic<address><country key="CZ"></country></address></affiliation></author><author xml:id="author-0006" role="corresp"><persName><forename type="first">Ophir D.</forename><surname>Klein</surname></persName><email>Ophir.Klein@ucsf.edu</email><affiliation>Department of Orofacial Sciences, University of California, San Francisco, California<address><country key="US"></country></address></affiliation><affiliation>Department of Pediatrics, University of California, San Francisco, California<address><country key="US"></country></address></affiliation><affiliation>Institutes of Human Genetics and Regeneration Medicine, University of California, San Francisco, California<address><country key="US"></country></address></affiliation><affiliation>Renata Peterkova, Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, v.v.i., Videnska 1083, 14220 Prague, Czech Republic=== Ophir D. Klein, Departments of Orofacial Sciences and Pediatrics, University of California, San Francisco, CA 94143‐0442 USA===</affiliation></author><idno type="istex">ECB51DFAF6AA56FBA9FD37985D1C2498853C8161</idno><idno type="ark">ark:/67375/WNG-LSZL3TWZ-P</idno><idno type="DOI">10.1002/jez.b.21266</idno><idno type="unit">JEZ21266</idno><idno type="toTypesetVersion">file:JEZ.JEZ21266.pdf</idno></analytic><monogr><editor xml:id="editor-0000"><persName><forename type="first">Thimios</forename><surname>Mitsiadis</surname></persName></editor><editor xml:id="editor-0001"><persName><forename type="first">Herve</forename><surname>Lesot</surname></persName></editor><editor xml:id="editor-0002"><persName><forename type="first">Moya</forename><surname>Smith</surname></persName></editor><title level="j" type="main">Journal of Experimental Zoology Part B: Molecular and Developmental Evolution</title><title level="j" type="sub">Tooth Development in Evolution and Disease, Part 1</title><title level="j" type="alt">JOURNAL OF EXPERIMENTAL ZOOLOGY PART B: MOLECULAR AND DEVELOPMENTAL EVOLUTION</title><idno type="pISSN">1552-5007</idno><idno type="eISSN">1552-5015</idno><idno type="book-DOI">10.1002/(ISSN)1552-5015</idno><idno type="book-part-DOI">10.1002/jez.b.v312b:4</idno><idno type="product">JEZ</idno><imprint><biblScope unit="vol">312B</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="292">292</biblScope><biblScope unit="page" to="308">308</biblScope><biblScope unit="page-count">17</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-06-15"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head><p>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 <hi rend="italic">Spry2</hi>, 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 (R<hi rend="subscript">2</hi>) and the first molar in the mandibles of <hi rend="italic">Spry2</hi><hi rend="superscript">−/−</hi> and wild‐type (WT) embryos using histological sections, image analysis and 3D reconstructions. In the WT R<hi rend="subscript">2</hi> 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 <hi rend="italic">Spry2</hi><hi rend="superscript">−/−</hi> embryos led to significantly decreased apoptosis and increased proliferation in the R<hi rend="subscript">2</hi> bud. Consequently, the R<hi rend="subscript">2</hi> 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. <hi rend="italic">J. Exp. Zool. (Mol. Dev. Evol.) 312B:292–308, 2009</hi>. © 2009 Wiley‐Liss, Inc.</p></abstract><textClass><keywords rend="articleCategory"><term>Research Article</term></keywords><keywords rend="tocHeading1"><term>Research Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/ECB51DFAF6AA56FBA9FD37985D1C2498853C8161/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1552-5015</doi><issn type="print">1552-5007</issn><issn type="electronic">1552-5015</issn><idGroup><id type="product" value="JEZ"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF EXPERIMENTAL ZOOLOGY PART B: MOLECULAR AND DEVELOPMENTAL EVOLUTION">Journal of Experimental Zoology Part B: Molecular and Developmental Evolution</title><title type="short">J. 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Klein, Departments of Orofacial Sciences and Pediatrics, University of California, San Francisco, CA 94143‐0442 USA===</line></lineatedText></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JEZ.JEZ21266.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="8"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="64"></count></countGroup><titleGroup><title type="main" xml:lang="en">Revitalization of a diastemal tooth primordium in <i>Spry2</i> null mice results from increased proliferation and decreased apoptosis</title><title type="short" xml:lang="en">REVITALIZATION OF DIASTEMAL TOOTH PRIMORDIUM</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Renata</givenNames><familyName>Peterkova</familyName></personName><contactDetails><email>repete@biomed.cas.cz</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Svatava</givenNames><familyName>Churava</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3 #af4 #af5"><personName><givenNames>Herve</givenNames><familyName>Lesot</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1 #af6"><personName><givenNames>Michaela</givenNames><familyName>Rothova</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1 #af6"><personName><givenNames>Jan</givenNames><familyName>Prochazka</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Miroslav</givenNames><familyName>Peterka</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af7 #af8 #af9" corresponding="yes"><personName><givenNames>Ophir D.</givenNames><familyName>Klein</familyName></personName><contactDetails><email>Ophir.Klein@ucsf.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CZ" type="organization"><unparsedAffiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="CZ" type="organization"><unparsedAffiliation>Department of Anthropology, Faculty of Science, Charles University, Prague, Czech Republic</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FR" type="organization"><unparsedAffiliation>INSERM U595, Faculté de Médecine, Université Louis Pasteur, Strasbourg, France</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="FR" type="organization"><unparsedAffiliation>Faculté de Chirurgie Dentaire, Université Louis Pasteur, Strasbourg, France</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="GB" type="organization"><unparsedAffiliation>International Collaborating Centre in Oro‐Facial Genetics and Development, University of Liverpool, Liverpool, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="CZ" type="organization"><unparsedAffiliation>Department of Developmental Biology, Faculty of Science, Charles University, Prague, Czech Republic</unparsedAffiliation></affiliation><affiliation xml:id="af7" countryCode="US" type="organization"><unparsedAffiliation>Department of Orofacial Sciences, University of California, San Francisco, California</unparsedAffiliation></affiliation><affiliation xml:id="af8" countryCode="US" type="organization"><unparsedAffiliation>Department of Pediatrics, University of California, San Francisco, California</unparsedAffiliation></affiliation><affiliation xml:id="af9" countryCode="US" type="organization"><unparsedAffiliation>Institutes of Human Genetics and Regeneration Medicine, University of California, San Francisco, California</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>Grant Agency of the Czech Republic</fundingAgency><fundingNumber>304/05/2665</fundingNumber><fundingNumber>304/07/0223</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Ministry of Education, Youth and Sports of the Czech Republic</fundingAgency><fundingNumber>MSM0021620843</fundingNumber><fundingNumber>COST B23.002</fundingNumber></fundingInfo><fundingInfo><fundingAgency>U.C.S.F. Sandler Family Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>NIH</fundingAgency><fundingNumber>K08‐DE017654</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>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 <i>Spry2</i>, 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 (R<sub>2</sub>) and the first molar in the mandibles of <i>Spry2</i><sup>−/−</sup> and wild‐type (WT) embryos using histological sections, image analysis and 3D reconstructions. In the WT R<sub>2</sub> 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 <i>Spry2</i><sup>−/−</sup> embryos led to significantly decreased apoptosis and increased proliferation in the R<sub>2</sub> bud. Consequently, the R<sub>2</sub> 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. <i>J. Exp. Zool. (Mol. Dev. Evol.) 312B:292–308, 2009</i>. © 2009 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Revitalization of a diastemal tooth primordium in Spry2 null mice results from increased proliferation and decreased apoptosis</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>REVITALIZATION OF DIASTEMAL TOOTH PRIMORDIUM</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Revitalization of a diastemal tooth primordium in Spry2 null mice results from increased proliferation and decreased apoptosis</title></titleInfo><name type="personal"><namePart type="given">Renata</namePart><namePart type="family">Peterkova</namePart><affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</affiliation><affiliation>E-mail: repete@biomed.cas.cz</affiliation><affiliation>Renata Peterkova, Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, v.v.i., Videnska 1083, 14220 Prague, Czech Republic===Ophir D. Klein, Departments of Orofacial Sciences and Pediatrics, University of California, San Francisco, CA 94143‐0442 USA===</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Svatava</namePart><namePart type="family">Churava</namePart><affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</affiliation><affiliation>Department of Anthropology, Faculty of Science, Charles University, Prague, Czech Republic</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Herve</namePart><namePart type="family">Lesot</namePart><affiliation>INSERM U595, Faculté de Médecine, Université Louis Pasteur, Strasbourg, France</affiliation><affiliation>Faculté de Chirurgie Dentaire, Université Louis Pasteur, Strasbourg, France</affiliation><affiliation>International Collaborating Centre in Oro‐Facial Genetics and Development, University of Liverpool, Liverpool, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michaela</namePart><namePart type="family">Rothova</namePart><affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</affiliation><affiliation>Department of Developmental Biology, Faculty of Science, Charles University, Prague, Czech Republic</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan</namePart><namePart type="family">Prochazka</namePart><affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</affiliation><affiliation>Department of Developmental Biology, Faculty of Science, Charles University, Prague, Czech Republic</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Miroslav</namePart><namePart type="family">Peterka</namePart><affiliation>Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic</affiliation><affiliation>Department of Anthropology, Faculty of Science, Charles University, Prague, Czech Republic</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ophir D.</namePart><namePart type="family">Klein</namePart><affiliation>Department of Orofacial Sciences, University of California, San Francisco, California</affiliation><affiliation>Department of Pediatrics, University of California, San Francisco, California</affiliation><affiliation>Institutes of Human Genetics and Regeneration Medicine, University of California, San Francisco, California</affiliation><affiliation>E-mail: Ophir.Klein@ucsf.edu</affiliation><affiliation>Renata Peterkova, Department of Teratology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, v.v.i., Videnska 1083, 14220 Prague, Czech Republic===Ophir D. Klein, Departments of Orofacial Sciences and Pediatrics, University of California, San Francisco, CA 94143‐0442 USA===</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009-06-15</dateIssued><dateCaptured encoding="w3cdtf">2008-11-19</dateCaptured><dateValid encoding="w3cdtf">2008-11-20</dateValid><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">8</extent><extent unit="tables">2</extent><extent unit="references">64</extent></physicalDescription><abstract 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.</abstract><note type="funding">Grant Agency of the Czech Republic - No. 304/05/2665; No. 304/07/0223; </note><note type="funding">Ministry of Education, Youth and Sports of the Czech Republic - No. MSM0021620843; No. COST B23.002; </note><note type="funding">U.C.S.F. Sandler Family Foundation</note><note type="funding">NIH - No. K08‐DE017654; </note><relatedItem type="host"><titleInfo><title>Journal of Experimental Zoology Part B: Molecular and Developmental Evolution</title></titleInfo><titleInfo type="abbreviated"><title>J. Exp. 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