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The cellular basis for epithelial-mesenchymal interaction during mouse tooth development

ABSTRACT: In this study, using mouse molar as the model, we developed a dual fluorescence reporter mouse to precisely track and analyze dental epithelium and mesenchyme at single-cell resolution from early embryonic to postnatal stages. Moreover, we constructed the virtual molar explorer (VMEx) to spatially map 15,967 molar-expressed genes and identified that Msx1+ Sdc1+ marked the developing dental papilla while surrounded by Msx1+ Sdc1- molar niche. Through tooth germ reconstitution and organoid culture in vitro and kidney capsule transplantation in vivo, we provided evidence that the Msx1+ Sdc1- dental follicle cells might function as the tooth organizers that promoted epithelium survival and tooth germ organization. Furthermore, the appearance of Msx1+ Sdc1+ dental papilla cells relied on the interaction between dental epithelium and Msx1+ Sdc1- dental follicle cells. Together, our results revealed the cellular dynamics of tooth development in mice and identified that the dental follicle might be the key driver of epithelial-mesenchymal interaction and tooth morphogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE162413 | GEO | 2022/11/01

REPOSITORIES: GEO

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Project description:Previous studies have suggested that Bmp4 is a key Msx1-dependent mesenchymal odontogenic signal for driving tooth morphogenesis through the bud-to-cap transition. Whereas the bud stage tooth developmental arrest in Msx1-/- mutant mice was accompanied by reduction in mesenchymal Bmp4 mRNA expression, we show that depleting functional Bmp4 mRNAs in the tooth mesenchyme, through neural crest-specific gene inactivation in Bmp4f/f;Wnt1Cre mice, caused mandibular molar developmental arrest at the bud stage but allowed maxillary molars and incisors to develop to mineralized teeth. We show that the Wnt inhibitors Dkk2 and Wif1 were much more abundantly expressed in the mandibular than maxillary molar mesenchyme in wildtype embryos and that Dkk2 expression was significantly unregulated in the tooth mesenchyme in Bmp4f/f;Wnt1Cre embryos. In addition, expression of Osr2, which encodes a zinc finger protein that antagonizes Msx1-mediated activation of odontogenic mesenchyme, is significantly upregulated in the molar mesenchyme in Bmp4f/f;Wnt1Cre embryos. Msx1 heterozygosity enhanced maxillary molar developmental defects whereas Osr2 heterozygosity rescued mandibular first molar morphogenesis in Bmp4f/f;Wnt1Cre mice. Moreover, in contrast to complete lack of supernumerary tooth initiation in Msx1-/-Osr2-/- mutant mice, Osr2-/-Bmp4f/f;Wnt1Cre compound mutant mice exhibit formation and subsequent arrest of supernumerary tooth germs that correlated with down regulation of Msx1 expression in the tooth mesenchyme. Taken together, our data indicate that, while reduction in mesenchymal Bmp4 expression alone could not account for the tooth bud arrest phenotype in Msx1-/- mutant mice, Bmp4 signaling synergizes with Msx1 and antagonizes Osr2 to activate mesenchymal odontogenic activity to drive tooth morphogenesis and sequential tooth formation. E13.5 mouse embryos tooth germs were microdissected by laser capture microdissection (LCM), and the mandibular molar and maxillary molar were separated. 3 pairs of control and mutant samples were pooled for the RNA extraction.

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The cellular basis for epithelial-mesenchymal interaction during mouse tooth development

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