Extended Data Fig. 3: ChIP–seq reveals binding patterns of NUP98–HOXA9 that carries either wild-type or an Phe-to-Ser mutated IDR.
From: Phase separation drives aberrant chromatin looping and cancer development
a, Summary of the counts of ChIP–seq read tags for the indicated samples. b, Scatterplots showing correlation of global N-IDRWT/A9 (left) or N-IDRFS/A9 (right) ChIP–seq signals using either HA (x axis) or GFP (y axis) antibodies in two biological replicates of 293FT stable cells. Coefficient of determination (R2) is determined by Pearson correlation. c, Total number of the called HA ChIP–seq peaks in stable 293FT cell lines expressing HA-tagged N-IDRWT/A9 (left) or N-IDRFS/A9 (middle) or empty vector control (right). d, e, Pie chart showing distribution of the indicated annotation feature among the called N-IDRWT/A9 (d) or N-IDRFS/A9 (e) ChIP–seq peaks in 293FT stable expression cells. f, g, Summary of the most enriched motifs identified within the called N-IDRWT/A9 (f) or N-IDRFS/A9 (g) ChIP–seq peaks in 293FT stable expression cells. Motif enrichment was statistically determined by ZOOPS scoring (zero or one occurrence per sequence) coupled with the hypergeometric enrichment calculations. h, Gene Ontology analysis of genes associated with broad super-enhancer-like peaks of N-IDRWT/A9 as identified in 293FT stable cells. P values were determined by Fisher’s exact test.
