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Molar tooth development in caspase-3 deficient mice
Matalova E, Sharpe PT, Lakhani SA, Roth KA, Flavell RA, Setkova J, Misek I, Tucker AS.
Jazyk angličtina Země Španělsko
PubMed
16586350
DOI
10.1387/ijdb.052117em
Knihovny.cz E-zdroje
- MeSH
- apoptóza MeSH
- fibroblastový růstový faktor 4 genetika MeSH
- financování organizované MeSH
- hybridizace in situ MeSH
- kaspasa 3 MeSH
- kaspasy genetika nedostatek MeSH
- messenger RNA metabolismus MeSH
- moláry cytologie embryologie enzymologie MeSH
- myši knockoutované MeSH
- myši MeSH
- odontogeneze fyziologie genetika MeSH
- proliferace buněk MeSH
- proteiny hedgehog MeSH
- trans-aktivátory genetika MeSH
- vývojová regulace genové exprese MeSH
- zubní sklovina cytologie embryologie enzymologie MeSH
- zubní zárodek cytologie embryologie enzymologie MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
Tooth morphogenesis is accompanied by apoptotic events which show restricted temporospatial patterns suggesting multiple roles in odontogenesis. Dental apoptosis seems to be caspase dependent and caspase-3 has been shown to be activated during dental apoptosis.Caspase-3 mutant mice on different genetic backgrounds were used to investigate alterations in dental apoptosis and molar tooth morphogenesis. Mouse embryos at E15.5 were analyzed to reveal any changes in enamel knots, which are transient structures eliminated by apoptosis. In caspase-3(-/-) mice on the B57BL/6 background, disorganization of the epithelium was found in the original primary enamel knot area and confirmed by altered expression of Shh. Despite this early defect in molar tooth development, these mutants showed correct formation of secondary enamel knots as indicated by Fgf-4 expression. Analyses of adult molar teeth did not reveal any major alterations in tooth shape, enamel structure or pattern when compared to heterozygote littermates. In caspase-3(-/-) mice on the 129X1/SvJ background, no defects in tooth development were found except the position of the upper molars which developed more posteriorly in the oral cavity. This is likely, however, to be a secondary defect caused by a physical squashing of the face by the malformed brain. The results suggest that although caspase-3 becomes activated and may be essential for dental apoptosis, it does not seem fundamental for formation of normal mineralised molar teeth.
Citace poskytuje Crossref.org
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