Fig. 6
Genetic variation identifies DNA motifs that promote accessible chromatin at TF binding sites. a Model describing the undifferentiated GATA2highGATA1low and the differentiated GATA2lowGATA1high erythroid states and the roles these TFs may play in regulating chromatin accessibility. b TFs whose motifs significantly alter genome-wide DNase peak signal (% impact, median ± 95% CI) when disrupted by a discSNP in undifferentiated (−GATA1) or differentiated (+GATA1) erythroid cells. Vertical line indicates no effect, and color indicates significance level. c TFs whose motifs significantly alter DNase signal (% impact, median ± 95% CI) at GATA1-regulated promoters or within TF binding peaks when disrupted by a discSNP in undifferentiated (−GATA1) or differentiated (+GATA1) erythroid cells. d Mean ChIP-seq intensity of GATA2 (in undifferentiated erythroid cells) at DNase peaks bound by GATA1 (in differentiated cells) at either an intact GATA motif or at one disrupted by a discSNP. Position is shown relative to the discSNP position (−400 bp upstream to 400 bp downstream). Significant differential binding (*) was assessed by BH-corrected Wilcoxon's test in the −200 to +200 region (q = 0.003). e Heatmaps showing the intensity of either GATA2 or GATA1 binding or DNase hypersensitivity in the undifferentiated (−GATA1) or differentiated (+GATA1) state at all sites that GATA1 binds in differentiated cells. Peaks (15,527) were sorted by GATA1 binding intensity in the differentiated state, regions span −1 kb to +1 kb centered on peak
