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. 2015 Mar 30;112(15):E1936–E1945. doi: 10.1073/pnas.1421480112

Fig. 2.

Fig. 2.

Loss of SOX2 Increases polycomb complex PRC2 activity at bivalent genes required for neuronal differentiation. (A) ChIP-seq plot of H3K4me3, H3K27me3, and SOX2 at Sox21, Bdnf, and Gadd45b loci in mouse NPCs. (B) SOX2 binding at Sox21, Bdnf, and Gadd45b loci in mouse adult hipNPCs. (C) H3K27me3 level at regulatory regions of Sox21 (Left), Bdnf (Center), and Gadd45b (Right) loci in mouse adult hipNPCs induced with shCTRL or shSox2. Highlighted is SOX2 binding at these promoters. (D) EZH2 binding in SOX2-binding sites of Ngn2, NeuroD1, Sox21, Bdnf, and Gadd45b loci in mouse hipNPCs. (E) Western blot showing H3K27me3 and EZH2 levels in SOX2-deficient and wild-type hipNPCs. (F, Left) Schematic of a 7-d cell-culture protocol used to differentiate SOX2-deficient hipNPCs under neurogenic signals (Wnt3a). (Right) Quantification of Sox21, Bdnf, and Gadd45b mRNA levels in adult hipNPCs under self-renewal or neurogenic signals (Wnt3a). For all quantifications, data are plotted as the mean ± SEM (*P < 0.05, **P < 0.01, ***P < 0.001).