Molar tooth development in caspase-3 deficient mice
Language English Country Spain Media print
Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't
Grant support
NS41962
NINDS NIH HHS - United States
PubMed
16586350
DOI
10.1387/ijdb.052117em
PII: 052117em
Knihovny.cz E-resources
- MeSH
- Apoptosis MeSH
- Fibroblast Growth Factor 4 genetics MeSH
- In Situ Hybridization MeSH
- Caspase 3 MeSH
- Caspases deficiency genetics MeSH
- RNA, Messenger genetics metabolism MeSH
- Molar cytology embryology enzymology MeSH
- Mice, Knockout MeSH
- Mice MeSH
- Odontogenesis genetics physiology MeSH
- Cell Proliferation MeSH
- Hedgehog Proteins MeSH
- Trans-Activators genetics MeSH
- Gene Expression Regulation, Developmental MeSH
- Dental Enamel cytology embryology enzymology MeSH
- Tooth Germ cytology embryology enzymology MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
- Names of Substances
- Casp3 protein, mouse MeSH Browser
- Fgf4 protein, mouse MeSH Browser
- Fibroblast Growth Factor 4 MeSH
- Caspase 3 MeSH
- Caspases MeSH
- RNA, Messenger MeSH
- Hedgehog Proteins MeSH
- Shh protein, mouse MeSH Browser
- Trans-Activators 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.
References provided by Crossref.org
Exploring caspase functions in mouse models
Making the head: Caspases in life and death
Role of Cell Death in Cellular Processes During Odontogenesis
Apoptotic signaling in mouse odontogenesis