Fig. 1

ASCL1 overexpression leads to association with de novo binding sites. a Average profile (top) and aligned heatmap (bottom) showing relative levels of endogenous and overexpressed WT ASCL1 binding at ASCL1 peaks identified in NB cells with endogenous ASCL1, or with overexpressed ASCL1 after 24 h induction with 1 μg/ml doxycycline (n = 8). Recruited peaks were called only in overexpressed conditions, whereas endogenous peaks were present in both endogenous and overexpressed conditions. Shown alongside, endogenous histone modification data from SH-SY5Y cells (H3K27ac, H3K4me1, H3K4me3, H3K27me3) or LAN6 cells (H3K9me3) [30, 31]. Data shown ± 3 kb from the peak centre. b Barchart showing the percentage of endogenous and recruited peaks that fall within NB gene promoters, enhancers, intergenic regions, and gene bodies. Actual number of peaks shown in each bar. c Top E-box binding motif identified in ASCL1 peaks with endogenous (endogenous motif), or overexpressed ASCL1 (recruited motif), against a background of random sequences matched for GC content. d Stacked barplot showing the proportion of endogenous and recruited ASCL1 peaks containing the E-box motifs CAGCTG and/or CAGGTG, or neither motif. Actual number of peaks shown in each segment. e Top E-box binding motif identified in top 1000 ASCL1 peaks from mouse NPC neuronal precursor cells (NPCs) and mouse embryonic fibroblasts (MEFs) induced for ASCL1 overexpression [25], against a background of random sequences matched for GC content