Fig. 1: Epithelial sensing of muscarinic receptor blockade results in selective DCLK1-positive tuft cell expansion.
From: Prox1-positive cells monitor and sustain the murine intestinal epithelial cholinergic niche
a, b Histologic analysis of WT (untreated) and scopolamine-treated WT (6 weeks) murine jejunal tissues. Scopolamine treatment provoked selective expansion of DCLK1-positive tuft cells (WT untreated (n = 5), Mean = 0.77, SEM = 0.080; WT + scopolamine 6 weeks (n = 6), Mean = 5.281, SEM = 0.543; unpaired t test, two-tailed, t = 7.453, df = 9); bar graphs left H&E, DCLK1 = 50 µm, magnifications H&E, DCLK1 right = 25 µm. c mRNA analysis of epithelial-enriched jejunal preparations for muscarinic receptors M1R—M5R (Chrm1—Chrm5) showed predominant expression of M3R and M1R (n = 6 WT mice). d Analysis of heterozygous M3R-KO mice (whole body-KO) showed significant DCLK1-positive tuft cell expansion (n = 5 WT mice, Mean = 0.77, SEM = 0.080; n = 3 M3R-KO mice, Mean = 3.467, SEM = 0.524; unpaired t test, two-tailed, t = 6.790, df = 6); bar graphs = 100 µm. e Tuft cell expansion similarly resulted from epithelial ablation of M3R employing Vil-Cre × M3R fl/fl mice (n = 5 WT mice, Mean = 0.77, SEM = 0.080; n = 6 Vil-Cre × M3R fl/fl −/− mice, Mean = 4.517, SEM = 0.377; unpaired t test, two-tailed, t = 8.848, df = 9); bar graphs = 100 µm. f Epithelial ablation of M1R employing Vil-Cre × M1R fl/fl mice resulted in modest DCLK1-positive tuft cell expansion (n = 3 mice each group, WT Mean = 0.7, SEM = 0.115; Vil-Cre × M1R fl/fl −/− Mean = 2.733, SEM = 0.367; unpaired t test, two-tailed, t = 5.280, df = 4); bar graphs = 100 µm. Source data are provided as a Source Data file. **p < 0.01, ***p < 0.005, ****p < 0.001.
