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. Author manuscript; available in PMC: 2015 Oct 1.
Published in final edited form as: Nat Med. 2015 Mar 30;21(4):335–343. doi: 10.1038/nm.3832

Figure 4.

Figure 4

Unique H3K9 epigenomic signature at MLL-AF9 bound gene loci in MLL-fusion leukemia. (a,b) Scatterplots showing ChIP-seq signals for H3K79me2 (x-axis) and H3K9ac (y-axis) in mouse (a) MLL-AF9 leukemic cells, and (b) LSK cells sorted from normal mouse bone marrow. Hoxa cluster genes and Meis1 are highlighted in black circles. (c,h) Screen shots showing ChIP-seq profiles of MLL-AF9 fusion protein (black), H3K79me2 (blue) and H3K9ac (red) at select MLL-AF9 bound target (HOXA cluster and MEIS1), active gene (GAPDH) and silent gene (HBB/OLFR) loci in (c) mouse and (h) human MLL-AF9 leukemic cell lines. The core occupied regions for MLL-AF9 fusion protein in mouse MLL-AF9 leukemia are highlighted (c; green-dashed box). (d–g) Boxplots showing ChIP-seq signal of H3K9ac in (d) mouse and (e–g) human MLL-AF9 leukemic cells including (e) Molm13, (f) Nomo1 and (g) MonoMac6 cells. (a,b,d–g) Data showing ChIP-seq signals of H3K79me2 or H3K9ac at TSS ± 2 kb regions of genome (gray; 18,240 genes), active genes (red; 4,560 genes), MLL-AF9 targets (green; 129 genes) and silent genes (blue; 4,560 genes). (d–g) Data represent mean ± s.d. *P < 0.001 to MLL-AF9 targets using Welch’s t-test.