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. Author manuscript; available in PMC: 2017 Sep 22.
Published in final edited form as: Cell Rep. 2017 Mar 7;18(10):2359–2372. doi: 10.1016/j.celrep.2017.02.025

Figure 3.

Figure 3

MEN1-dependent H3K4me3 and differential expression at selected target genes

(A) Immunoblot of H3K4me3 in histone extracts from shCtrl and shMEN1#1 cells. Histone H3 protein levels were used as an internal control. Silencing of MEN1 in the corresponding total cell lysate is also shown.

(B) Venn diagram of H3K4me3 ChIP-seq peaks after shCtrl and shMEN1 in vehicle treated cells.

(C) Average H3K4me3 ChIP-seq signals at TSS without menin and with menin peaks after shCtrl or shMEN1 induction.

(D) Gene expression at TSS without menin and bound by menin after MEN1 silencing (no significant differences between shCtrl and shMEN1).

(E) Waterfall plot of H3K4me3 ChIP-seq fold changes after MEN1 silencing at menin-bound TSS. TSS that have higher H3K4me3 levels in shCtrl cells are potential menin-H3K4me3-dependent genes.

(F) Heat map of average fold change of significantly down regulated transcripts after MEN1 silencing (Limma, <0.5 log2 fold down, P<0.01, RPKM>1)

(G) Overlap of down regulated transcripts (Limma, <-0.5 log2, p<0.05) after treatment with the menin-MLL1 inhibitor MI-2 or shMEN1#1.

(H) Heat map showing transcripts of 57 genes that are significantly down regulated by both MI-2 and shMEN1#1 (experiments in duplicate).