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. Author manuscript; available in PMC: 2012 Aug 6.
Published in final edited form as: Nat Med. 2012 Feb 6;18(2):298–301. doi: 10.1038/nm.2651

Figure 4.

Figure 4

Notch1 binding mediates loss of H3K27me3 and eviction of PRC2 in T-ALL. (a) Enrichment of Notch1 binding sites around TSSs characterized by each indicated histone mark. (b) H3K27me3 average signal profiles around TSS areas (blue line: Notch1-bound genes, gray line: genes not-bound by Notch1). (c) ChIP for H3K27me3 in a T-ALL cell line (CUTLL1) treated with γSI. The Loucy T-ALL line is used as a negative control. (d) HES1 expression in the indicated cell lines and normal human thymocytes and ChIP for H3K27me3 in the indicated cell lines and primary cells. (e) High leukemogenic potential of the human T-ALL samples in xenograft models. Spleen sections of recipient mice stained with an hCD45 antibody or an IgG control. (f) qPCR for HES1 expression and the levels of H3K27me3 in primary human T-ALL samples and human thymocytes (P<0.0001 between M69 and the human thymus). (g) ChIP experiments for Ezh2 on the Hes1 promoter in DP (green) and T-ALL (red). (h) Suz12 binding on the Hes1 promoter. (i)γSI-mediated changes of the N1-IC levels modulate JARID2 recruitment to the HES1 promoter (P=0.059).