Apoptotic Signaling in Mouse Odontogenesis

Matalová, Eva; Švandová, Eva; Tucker, Abigail S.

doi:10.1089/omi.2011.0039

Cited by 27 publications

(33 citation statements)

References 122 publications

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“…In WT embryos, cell death is specifically concentrated in the posterior part of the upper and lower diastema, where the large premolar buds regress (Peterkova et al, ; Lesot et al, ; Viriot et al, ). Specific concentration of apoptosis also occurs in the enamel knot of molars (Lesot et al, ; Vaahtokari et al, ; Matalova et al, ; Matalova et al, ) and in the anterior portion of M1 epithelium from ED14.5 (Lesot et al, ; Viriot et al, ).…”

Section: Discussionmentioning

confidence: 99%

The Dynamics of Supernumerary Tooth Development Are Differentially Regulated by Sprouty Genes

et al. 2013

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In mice, a toothless diastema separates the single incisor from the three molars in each dental quadrant. In the prospective diastema of the embryo, small rudimentary buds are found that are presumed to be rudiments of suppressed teeth. A supernumerary tooth occurs in the diastema of adult mice carrying mutations in either Spry2 or Spry4. In the case of Spry2 mutants, the origin of the supernumerary tooth involves the revitalization of a rudimentary tooth bud (called R2), whereas its origin in the Spry4 mutants is not known. In addition to R2, another rudimentary primordium (called MS) arises more anteriorly in the prospective diastema. We investigated the participation of both rudiments (MS and R2) in supernumerary tooth development in Spry2 and Spry4 mutants by comparing morphogenesis, proliferation, apoptosis, size and Shh expression in the dental epithelium of MS and R2 rudiments. Increased proliferation and decreased apoptosis were found in MS and R2 at embryonic day (ED) 12.5 and 13.5 in Spry2(-/-) embryos. Apoptosis was also decreased in both rudiments in Spry4(-/-) embryos, but the proliferation was lower (similar to WT mice), and supernumerary tooth development was accelerated, exhibiting a cap stage by ED13.5. Compared to Spry2(-/-) mice, a high number of Spry4(-/-) supernumerary tooth primordia degenerated after ED13.5, resulting in a low percentage of supernumerary teeth in adults. We propose that Sprouty genes were implicated during evolution in reduction of the cheek teeth in Muridae, and their deletion can reveal ancestral stages of murine dental evolution.

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Section: Discussionmentioning

confidence: 99%

The Dynamics of Supernumerary Tooth Development Are Differentially Regulated by Sprouty Genes

et al. 2013

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“…FasL binds to its receptor Fas, which induces apoptosis. In early stage of morphogenesis dental epithelium expresses both Fas and FasL, but very little information is available on expression of these factors at later stages of amelogenesis. Ameloblasts in secretory and maturation stage did not immunostain for TNFα but were positive for Fas .…”

Section: Discussionmentioning

confidence: 99%

The Intramembrane Protease SPPL2A Is Critical for Tooth Enamel Formation

Bronckers

Gueneli

Lüllmann‐Rauch

et al. 2013

Journal of Bone and Mineral Research

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Intramembrane proteases are critically involved in signal transduction and membrane protein turnover. Signal-peptide-peptidase-like 2a (SPPL2A), a presenilin-homologue residing in lysosomes/late endosomes, cleaves type II-oriented transmembrane proteins. We recently identified SPPL2A as the enzyme controlling turnover and functions of the invariant chain (CD74) of the major histocompatibility complex II (MHCII) and demonstrated critical importance of this process for B cell development. Surprisingly, we found that SPPL2A is critical for formation of dental enamel. In Sppl2a knockout mice, enamel of the erupted incisors was chalky white and rapidly eroded after eruption. SPPL2A was found to be expressed in enamel epithelium during secretory and maturation stage amelogenesis. Mineral content of enamel in Sppl2a À/À incisors was inhomogeneous and reduced by $20% compared to wild-type mice with the most pronounced reduction at the mesial side. Frequently, disruption of the enamel layer and localized detachment of the most superficial enamel layer was observed in the knockout incisors leading to an uneven enamel surface. In Sppl2a null mice, morphology and function of secretory stage ameloblasts were not noticeably different from that of wild-type mice. However, maturation stage ameloblasts showed reduced height and a characteristic undulation of the ameloblast layer with localized adherence of the cells to the outer enamel. This was reflected in a delayed and incomplete resorption of the proteinaceous enamel matrix. Thus, we conclude that intramembrane proteolysis by SPPL2A is essential for maintaining cellular homeostasis of ameloblasts. Because modulation of SPPL2A activity appears to be an attractive therapeutic target to deplete B cells and treat autoimmunity, interference with tooth enamel formation should be investigated as a possible adverse effect of pharmacological SPPL2A inhibitors in humans.

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“…Furthermore, based on these studies, Hall hypothesized that the inductive cue for conjunctival papillae development may reside within the underlying mesenchyme. As such, the conjunctival papillae and the underlying scleral skeletogenic condensations represent a reciprocal system similar to those that have been described in both hair and tooth development (Eames and Schneider, ; Drew et al, ; Duverger and Morasso, ; Koussoulakou et al, ; Catón and Tucker, ; Cobourne and Sharpe, ; Lin et al, ; Jiang et al, ; Porntaveetus et al, ; Matalova et al, ; Sennett and Rendl, ; Painter et al, ; Yue et al, ; Chuong et al, ).…”

Section: Introductionmentioning

confidence: 66%