Skip to main content
. Author manuscript; available in PMC: 2012 Jul 12.
Published in final edited form as: Cancer Cell. 2011 Jul 12;20(1):66–78. doi: 10.1016/j.ccr.2011.06.010

Figure 2. Relationship between H3K79me2 and other histone modifications on direct MLL-AF9 fusion targets.

Figure 2

(A) ChIP-Sequencing for H3K4me3, H3K27me3, H3K36me3, and H3K79me2, in sorted LSK, GMP and L-GMP populations. A screen shot of the HoxA cluster shows changes in these epigenetic marks during normal development (LSK and GMP), and in MLL-AF9 driven leukemogeneis (L-GMP). Also shown: MLL-AF9 fusion ChIP-Seq in MLL-AF9 tansformed cells (MLL-AF9-Bio); differential gene expression in L-GMP versus GMP as assessed by expression array (Expr L-GMP vs. GMP), color legend denotes fold change.

(B) Genome wide representation of the relation between H3K4me3 and H3K79me2 in LSK cells on fusion target genes (red) compared to non-fusion target genes (grey).

(C) Genome wide representation of the relation between H3K4me3 and H3K79me2 in L-GMP on fusion target genes (red) compared to non-fusion target genes (grey).

(D) Changes in expression between LSK and GMP (obtained by expression array, x-axis) in correlation to changes in H3K79me2 (Chip-seq, y-axis). This correlation is shown for MLL-AF9 targets in red, and non-targets in grey.

(E) Changes in expression between L-GMP and GMP in correlation with changes in H3K79me2. Shown is the amount of H3K79me2 signal difference for MLL-AF9 target genes (red) compared to genes that show similar differences in expression between L-GMP and GMP, but are not MLL-fusion targets (grey). See also Figure S2.