Establishment of crown–root domain borders in mouse incisor

Juuri, Emma; Saito, Kan; Lefebvre, Sylvie; Michon, Frédéric

doi:10.1016/j.gep.2013.05.001

Cited by 4 publications

(6 citation statements)

References 38 publications

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“…mitotic DNA replication, DNA replication initiation) (Table S4). We also found a number of genes important for the mineralisation of forming teeth, such as embigin (Xie et al, 2015), Six4 (Nonomura et al, 2010) and Cxcr4 (Juuri et al, 2013b), the last of which is thought to be important for the migration of epithelial progenitors in adult laCL (Yokohama-Tamaki et al, 2015). Also, Sox11, which is involved in palate development (Sock et al, 2004;Watanabe et al, 2016) and expressed in the mouse embryonic molar (Dy et al, 2008;Hargrave et al, 1997), was enriched by 4.40 fold.…”

Section: Modulation Of the Sox2 + Cell Signature In Embryonic Versus Adult Incisorsmentioning

confidence: 62%

“…Mmp13, Mmp14, Mmp20) (Table S1). We also detected expression of Barx2, a gene involved in cell migration and differentiation (Juuri et al, 2013b). Moreover, clusterin (Clu), a stress-activated and apoptosisassociated chaperone, which has been found in embryonic and postnatal mouse molars (Chou et al, 2009;Khan et al, 2013;Shiota et al, 2012), was enriched in adult Sox2 + cells by a fold change of 187.08.…”

Section: Modulation Of the Sox2 + Cell Signature In Embryonic Versus Adult Incisorsmentioning

confidence: 88%

“…As the Pitx2driven Sox2 cKO led to the absence of incisors at late stages of morphogenesis (Sun et al, 2016), we decided to use Shh Cre-GFP/+ to delete Sox2. Shh is expressed later than Pitx2, and almost all dental epithelial cells derive from early Shh + cells (Juuri et al, 2013b). The Shh-driven Sox2 cKO mice have a hyperplastic dental epithelium in the second and third molars (Juuri et al, 2013a), but no incisor phenotype has been described.…”

Section: Deletion Of Sox2 Leads To Incisor Defects During Morphogenesismentioning

confidence: 99%

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Plasticity within the niche ensures the maintenance of a Sox2+ stem cell population in the mouse incisor

Sanz-Navarro

Seidel²,

Sun

et al. 2018

Development

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In mice, the incisors grow throughout the animal's life, and this continuous renewal is driven by dental epithelial and mesenchymal stem cells. is a principal marker of the epithelial stem cells that reside in the mouse incisor stem cell niche, called the labial cervical loop, but relatively little is known about the role of the stem cell population. In this study, we show that conditional deletion of in the embryonic incisor epithelium leads to growth defects and impairment of ameloblast lineage commitment. Deletion of specifically in cells during incisor renewal revealed cellular plasticity that leads to the relatively rapid restoration of a-expressing cell population. Furthermore, we show that -expressing cells are a subpopulation of dental cells that also arise from cells during tooth formation. Finally, we show that the embryonic and adult populations are regulated by distinct signalling pathways, which is reflected in their distinct transcriptomic signatures. Together, our findings demonstrate that a stem cell population can be regenerated from cells, reinforcing its importance for incisor homeostasis.

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Section: Modulation Of the Sox2 + Cell Signature In Embryonic Versus Adult Incisorsmentioning

confidence: 62%

Section: Modulation Of the Sox2 + Cell Signature In Embryonic Versus Adult Incisorsmentioning

confidence: 88%

Section: Deletion Of Sox2 Leads To Incisor Defects During Morphogenesismentioning

confidence: 99%

See 1 more Smart Citation

Plasticity within the niche ensures the maintenance of a Sox2+ stem cell population in the mouse incisor

Sanz-Navarro

Seidel²,

Sun

et al. 2018

Development

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“…In contrast, the BMPRIA conditional KO mouse has defective tooth development and presents interruption of epithelial BMP signalling via BMPRIA depletion, which switches the differentiation of crown epithelia into the root lineage 26 . It has also been suggested that follistatin, a known BMP inhibitor, may also be involved in crown and root border formation 57 . In the present study, we chose to focus on the downstream phosphorylation of Smad1/5/8.…”

Section: Discussionmentioning

confidence: 99%

Mutant GDF5 enhances ameloblast differentiation via accelerated BMP2-induced Smad1/5/8 phosphorylation

Liu

Saito

Maruya

et al. 2016

Sci Rep

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Bone morphogenetic proteins (BMPs) regulate hard tissue formation, including bone and tooth. Growth differentiation factor 5 (GDF5), a known BMP, is expressed in cartilage and regulates chondrogenesis, and mutations have been shown to cause osteoarthritis. Notably, GDF5 is also expressed in periodontal ligament tissue; however, its role during tooth development is unclear. Here, we used cell culture and in vivo analyses to determine the role of GDF5 during tooth development. GDF5 and its associated BMP receptors are expressed at the protein and mRNA levels during postnatal tooth development, particularly at a stage associated with enamel formation. Furthermore, whereas BMP2 was observed to induce evidently the differentiation of enamel-forming ameloblasts, excess GDF5 induce mildly this differentiation. A mouse model harbouring a mutation in GDF5 (W408R) showed enhanced enamel formation in both the incisors and molars, but not in the tooth roots. Overexpression of the W408R GDF5 mutant protein was shown to induce BMP2-mediated mRNA expression of enamel matrix proteins and downstream phosphorylation of Smad1/5/8. These results suggest that mutant GDF5 enhances ameloblast differentiation via accelerated BMP2-signalling.

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“…1 Moreover, analysis of the labial side of mouse incisors is an invaluable tool for observing the differentiation process of the dental epithelium. 1,2 Recent advances in single-cell RNA-sequencing have facilitated mRNA analysis at the single-cell level, enabling the identification of molecules expressed in each cell. Ameloblasts are not monophasic and express different molecules depending on the stage of differentiation; expressing dentin sialophosphoprotein (Dspp) in the early stage of differentiation and strongly expressing ameloblastin (Ambn) in differentiated ameloblasts.…”

Section: Introductionmentioning

confidence: 99%

S100a6 knockdown promotes the differentiation of dental epithelial cells toward the epidermal lineage instead of the odontogenic lineage

Otake,

Saito,

Chiba

et al. 2024

The FASEB Journal

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Tooth development is a complex process involving various signaling pathways and genes. Recent findings suggest that ion channels and transporters, including the S100 family of calcium‐binding proteins, may be involved in tooth formation. However, our knowledge in this regard is limited. Therefore, this study aimed to investigate the expression of S100 family members and their functions during tooth formation. Tooth germs were extracted from the embryonic and post‐natal mice and the expression of S100a6 was examined. Additionally, the effects of S100a6 knockdown and calcium treatment on S100a6 expression and the proliferation of SF2 cells were examined. Microarrays and single‐cell RNA‐sequencing indicated that S100a6 was highly expressed in ameloblasts. Immunostaining of mouse tooth germs showed that S100a6 was expressed in ameloblasts but not in the undifferentiated dental epithelium. Additionally, S100a6 was localized to the calcification‐forming side in enamel‐forming ameloblasts. Moreover, siRNA‐mediated S100a6 knockdown in ameloblasts reduced intracellular calcium concentration and the expression of ameloblast marker genes, indicating that S100a6 is associated with ameloblast differentiation. Furthermore, S100a6 knockdown inhibited the ERK/PI3K signaling pathway, suppressed ameloblast proliferation, and promoted the differentiation of the dental epithelium toward epidermal lineage. Conclusively, S100a6 knockdown in the dental epithelium suppresses cell proliferation via calcium and intracellular signaling and promotes differentiation of the dental epithelium toward the epidermal lineage.

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Establishment of crown–root domain borders in mouse incisor

Cited by 4 publications

References 38 publications

Plasticity within the niche ensures the maintenance of a Sox2+ stem cell population in the mouse incisor

Plasticity within the niche ensures the maintenance of a Sox2+ stem cell population in the mouse incisor

Mutant GDF5 enhances ameloblast differentiation via accelerated BMP2-induced Smad1/5/8 phosphorylation

S100a6 knockdown promotes the differentiation of dental epithelial cells toward the epidermal lineage instead of the odontogenic lineage

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