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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 1.

Figure 1

The PRC2 complex as a tumor suppressor in T-ALL. (a) Structure of the EZH2 protein including 2 SANT DNA binding domains, the cysteine-rich CXC domain and the catalytic SET domain. Overview of all EZH2 mutations identified in primary T-ALL samples. Filled circles: nonsense and frameshift mutations, open circles: missense mutations. (b) Representative chromatograms of paired diagnosis and remission genomic DNA samples showing somatic mutations in exon 8 and exon 10 of EZH2. (c) Structure of the SUZ12 protein including a zinc finger domain and the VEFS domain. (d) Representative DNA sequencing chromatograms showing a frame-shift mutation in exon 10 of SUZ12 and of paired diagnosis and remission genomic DNA samples showing a somatic point mutation in exon 14 of this gene. (e) Pie-chart summarizing the frequencies of homozygous and heterozygous mutations of EZH2 and SUZ12 in adult TALL patients. (f) EZH2 protein levels in samples from patients (#1 and #4) with mutations and deletions on the EZH2 gene compared to WT controls. (g) Silencing of EZH2 and SUZ12 in the Jurkat human T-ALL line. HES1 and DTX1 mRNA expression levels followed silencing of either SUZ12 or EZH2. Knockdown of the luciferase (LUC) gene was used as a control.