Enrichment of C/EBPα and PU.1 at dynamic sites of chromatin accessibility upon LSD1 inhibition. (A) Top 3 motif signatures of GSK-LSD1–induced dynamic ATAC-seq peaks. (B) Plot showing the relative expression of PU.1 messenger RNA (mRNA) in MLL-AF9 leukemia cells treated with vehicle control (PBS) or 0.5 μM GSK-LSD1. (C) Plot showing the relative expression of C/EBPα mRNA in MLL-AF9 leukemia cells treated with vehicle control (PBS) or 0.5 μM GSK-LSD1. (D) Bar plot showing the number of peaks with either gains or losses of signal in ChIP-seq of PU.1 and C/EBPα in GSK-LSD1 treatment vs control. (E-F) Composite plots show normalized ChIP-seq signal at all dynamic ATAC sites in treatment and control for (E) PU.1 and (F) C/EBPα. (G) Genome browser track (mm9 coordinates chromosome 9: 14 425 541-14 466 000) showing normalized ATAC-seq and ChIP-seq signal under treatment and control conditions. (H) Percentage occupancy of PU.1 and C/EBPα in control and treatment conditions for ATAC-seq sites induced by GSK-LSD1. DMSO, dimethyl sulfoxide.