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. 2011 Jun;2(6):607–617. doi: 10.1177/1947601910393957

Figure 1.

Figure 1.

How the histone code may direct DNA methylation during development and carcinogenesis. (A) During normal development, the transcriptionally activating mark H3K4 me3 (x) blocks or repels DNMTs, whereas the repressive marks H3K9me or H3K27me (y) permit or recruit DNMTs, possibly by direct protein-protein interactions (e.g., EZH2-DNMTs). During carcinogenesis, disruption of the histone code in the form of (B) loss of H3K4me3 (x), (C) substitution of H3K4me3 with H3K9me or H3K27me (y), randomization of marks, aberrant acquisition of a new mark (z), or (D) loss of all histone marks permits or actively induces DNMT recruitment. x = H3K4me3; y = H3K9me or H3K27me; z = other histone mark; bent arrow = transcription start site; lollipops = histone marks; black circles = DNA methylation.