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. 2019 Jun 21;8(3):487–511. doi: 10.1016/j.jcmgh.2019.06.005

Figure 4.

Figure 4

Ductal deletion of Hnf1b leads to ADM and lipomatosis at P25. (A and B) H&E staining. Arrows show acini with increased lumen size in mutants, a feature of ADM. (C and D) Amylase (green) and Hnf1b (red) immunostaining. (E and F) Amylase (green) and Sox9 (red) immunostaining. (G and H) Amylase (green) and Hnf6 (red) immunostaining. Arrows show amylase+ cells with nuclear Hnf6+ staining, which is characteristic of ADM in mutants. (I) RT-qPCR of acinar markers. (J) RT-qPCR of Hnf6, Muc1, and Sox9. (K and L) Muc1 (green) and β-Cat (red) immunostaining. Muc1 staining is lost at the apical surface of ductal cells in mutants. (M and N) Amylase (green) and Pan-cytokeratin (red) immunostaining. (N’) PanCK localization is expanded in acinar cells of mutants. (O and P) FABP4 immunostaining shows adipocytes in mutants. (Q) RT-qPCR of YAP transcriptional targets (R) RT-qPCR of Notch signaling components. (S) RT-qPCR of TGF-β1 and P8/NuPr1. Scale bars: 50 μm. Nuclei are stained with 4′,6-diamidino-2-phenylindole (blue). Control, n ≥ 3; mutant, n ≥ 3 for immunostainings; and control, n = 7; mutant, n = 8 for RT-qPCR. *P < .05; **P < .01; and ***P < .001.