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Comparative study of gene expression in lower and upper first molar cap stage tooth germs of DUHi and FVB mice

ABSTRACT: The dataset aims at comparing gene expression in the developing lower and upper first molars of two mouse strains: DUHi and FVB. We studied molar tooth germ an early cap stage, looking for differences in activation-inhibition mechanisms that promote tooth formation. 19202 genes are in common between FVB and reference strain C57B6 and have a MGI annotation. Out of these genes, 2234 genes (11.6%) presented a significant difference of expression between the mapping on the reference strain C57B6 and the mapping on FVB strain (DESeq2, adjusted P value < 0.05, considering the mapping effect that is with 12 replicates). This is presumably a mapping artifact, due to the sequence divergence between mouse strains. These genes were removed, and the remaining 16,968 genes were retained for further analysis. 3619 genes were found to be differentially expressed between the two strains in the lower and upper molar (jaw+strain)

ORGANISM(S): Mus musculus

PROVIDER: GSE135432 | GEO | 2020/03/27

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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Comparative study of gene expression in lower and upper first molar cap stage tooth germs of DUHi and FVB mice

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