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. 2019 May 2;12(5):934–949. doi: 10.1016/j.stemcr.2019.04.007

Figure 6.

Figure 6

Chemical Activation of WNT Signaling Regulates MGE Progenitor Proliferation and Differentiation via Regulation of NOTCH Signaling

(A and B) CHIR99021 (2 μM) was added to the MGE progenitors to activate WNT/CTNNB1 signaling at days 17–25. At day 25, CHIR99021-treated MGE progenitors showed increased cell populations labeled with BrdU, Ki67, and PH3, but decreased cell populations labeled with DCX (A). Scale bar, 50 μm. Statistical results were shown in (B). n = 101–835 cells in at least three independent experiments; unpaired t test, ∗∗p < 0.01.

(C) At day 25, the MGE progenitors treated with or without CHIR99021 showed FOXG1 staining, but not HOXB4. Scale bar, 50 μm.

(D) The MGE progenitors with or without CHIR99021 were immunolabeled by NKX2.1 at day 25. Scale bar, 50 μm.

(E and F) DAPT significantly reduced the population of cells labeled with BrdU and Ki67 upon CHIR99021-triggered WNT/CTNNB1 signaling activation (E). Scale bar, 50 μm. Statistical results were shown (F). n = 110–569 cells in at least three independent experiments; unpaired t test, ∗∗p < 0.01, ∗∗∗p < 0.001.

(G) DAPT significantly rescued CHIR99021-induced reduction of neuronal genes, including DCX, TUJ1, and LHX6 expression in MGE progenitors. At least three independent experiments were performed; unpaired t test, ∗p < 0.05, ∗∗∗p < 0.001.