Fig. 2 |. ENL mutations enhance chromatin occupancy by ENL and associated SEC complex to enforce active transcription.

a, Heat map representation of ENL-bound chromatin peaks that show increased occupancy by T1, T 2 and T3 mutants compared with WT ENL (n = 54; Supplementary Table 6) in HEK293 cells. These heat maps are centred on ENL-bound peaks across a ±5-kb window. The colour key represents the signal density, with darker colour representing a more intense signal. b, GSEA plots showing that genes (n = 87; Supplementary Table 10) with enhanced occupancy by ENL mutants are upregulated in mutant-expressing HEK293 cells. c, Genome browser view of Flag–ENL, CDK9 and Pol II phosphorylated serine 2 (S2P) ChIP–seq signals at selected ENL target genes in HEK293 cells. d, e, Box plots showing log₂ fold changes (T mutants versus WT) in CDK9 (d) or Pol II S2P (e) ChIP–seq signals at genes that have enhanced binding of ENL mutants (mutants_up, n = 87; Supplementary Table 10) and at the other genes in the genome (others) in H EK293 cells. The indicated P-values were obtained by one-sided Wilcoxon signed-rank tests. For box plots, the centre lines represent the median; the box limits are the 25th and 75th percentiles; and the whiskers show the minimum to maximum values. f, Analysis of messenger RNA expression (normalized to GAPDH expression) from the indicated ENL-target genes in HEK293 cells that express the indicated ENL or vector constructs upon treatment with flavopiridol for 3 h. Increasing dosages (0, 10 nM, 100 nM and 1,000 nM) are depicted by grey wedge. Means ± s.e.m., n = 3 technical replicates. Data represent two independent experiments.