with representative peaks from each group shown in Figure 4C. The largest group, (Group I, 43%), consists of sites that gained significant H3K4me1 24 h after PU.1 activation. This gained H3K4me1 signal exhibited a bimodal spatial distribution identical to that observed for PU.1-associated H3K4me1 in macrophages and B cells (Figure S4A). Together with the fact that 90% of the sites that gain H3K4me1 are within a 1 kb window of a gained PU.1 site, these findings suggest that PU.1 binding is required to direct the local deposition of H3K4me1 at these sites. Group II (32%) consists of induced PU.1 binding sites that were marked by pre-existing H3K4me1. In this group, PU.1 binding initiated remodelling of the local H3K4me1-containing nucleosomes at 1 h and 24 h, again establishing a pattern identical to that in macrophages and B cells (Figure S4A). Group III (25%) consists of peaks that despite stable binding of PU.1 were not enriched for H3K4me1 at any time point, indicating that here, PU.1 binding is not sufficient to establish this mark. Increased recruitment of C/EBPβ to Groups I (37%) and II (30%) relative to Group III (11%) peaks (<100 bp) suggests that additional factors may be required for deposition
