Fig. 6: Foxl1-dependent telocyte signals impact epithelial gene expression in the fetal gut.
From: Villification of the intestinal epithelium is driven by Foxl1 through activation of PDGFRα and BMPs
A UMAP plot of control epithelial cells from E15.5 embryos. The cells partition into two major clusters of secretory progenitors (red) and undifferentiated epithelial cells (blue). B Heatmap of the 255 genes differentially expressed between secretory progenitors and undifferentiated epithelial cells. Each row represents a gene, each column a cell. C Expression of key marker genes in secretory progenitors and undifferentiated epithelial cells. D UMAP plot of control (green) and Foxl1 null (orange) epithelial cells. E Proportion of secretory progenitors and undifferentiated epithelial cells in control and Foxl1 null embryos. F Gene set enrichment analysis (GSEA) identifies critical pathways normally active in fetal small intestinal epithelial cells as Foxl1 dependent. G Staining of the fetal (15.5 dpc) small intestine with an antibody specific to Agr2 (Anterior gradient protein 2 homolog), a marker of the secretory lineage. H Staining of the fetal (15.5 dpc) small intestine with an antibody specific to Muc2 (Mucin 2), a marker of the goblet cell lineage. I Quantification of the proportion of Agr2-positive epithelial cells of all epithelial cells (DAPI/E-cadherin double positive) in the 15.5.dpc anterior small intestine. N = 3 embryos per genotype, p < 0.0001 by two-tailed unpaired t-test with Welch’s correction. J Quantification of the proportion of Muc2-positive epithelial cells of all epithelial cells (DAPI/E-cadherin double positive) in the 15.5. dpc anterior small intestine. N = 3 embryos per genotype. Data are presented as mean +/- standard deviation. p = 0.0002 by two-tailed unpaired t-test with Welch’s correction.
