Fig. 5: Loss of Smoc1/2 leads to quiescence loss and mesenchymal hierarchy disruption. | Nature Communications

Fig. 5: Loss of Smoc1/2 leads to quiescence loss and mesenchymal hierarchy disruption.

From: Autocrine ECM molecules establish MSC quiescence during incisor development by disrupting WNT ligand trafficking process

Fig. 5: Loss of Smoc1/2 leads to quiescence loss and mesenchymal hierarchy disruption.The alternative text for this image may have been generated using AI.

a–l Immunostaining of Ki67 and Sp7 in incisors of Smoc2+/- littermate control (control) and Smoc1/2 DKO mice at E13.5, E14.5 and E16.5. m, n Images of control and Smoc1/2 DKO embryos at E16.5. Scale bars: 50 μm in (a–l) and 1 cm in m, n. Representative images from three independent experiments with similar results. o–s Comparison of incisor mesenchymal populations in wild type control (control) and Smoc1/2 DKO mice. o, p UMAP plot of the incisor mesenchyme of wild type and Smoc1/2 DKO mice at E16.5. q Heatmap illustrating the top 10 differentially expressed genes between wild-type control and Smoc1/2 DKO incisor mesenchymal clusters. r The percentage of mesenchymal cell types in control and Smoc1/2 DKO mice. s UMAP feature plots in wild-type or Smoc1/2 DKO mice embryo showed apical pulp signature genes expression nearly diminished in the mutant incisor. t Feature plots of Mki67 and Sp7 in control and Smoc1/2 DKO incisor mesenchyme. u Quantitation of the expression level of Mki67 and Sp7 in individual cells within MSCs cluster of wild-type control and Smoc1/2 DKO. Two-tailed Mann–Whitney U test; Mki67: control vs DKO, p < 0.0001; Sp7: control vs DKO, p < 0.0001. Source data are provided as a Source Data file. v Mip-seq showing the RNA probe signals of Mki67 and Sp7 in the incisor of control and Smoc1/2 DKO mice. Scale bars: 50 μm. Representative images from three independent experiments with similar results.

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