Fig. 4

PU.1 overexpression drives modest chromatin accessibility changes. a Western blot showing PU.1 overexpression (OE) produces a protein of the same size as endogenous PU.1. β-actin used as loading control (n = 2 replicates). b PU.1 overexpressing and vector control K562 mean DNase-seq signal found ±1 kb from DHS site center for all SAHA-opened DHS sites split into those that contain a PU.1 binding site (ChIP-seq peak) and those that do not. Light gray shading = SEM (n = 2 replicates). c PU.1-bound, SAHA-opened DHS sites exhibit greater mean fold-change of DNase-seq signal upon PU.1 overexpression than PU.1-bound sites that do not open with SAHA or SAHA-opened DHS sites without PU.1 binding. The cumulative fraction of DHS sites with each level of accessibility change is depicted. Mann–Whitney tests used to assess significance of the shift in distributions. d Two example DHS sites (shaded in gray boxes) found in an intron of TMEM51. The first (left) represents a SAHA-opened DHS site that does not have a PU.1 ChIP peak and exhibits no increase in accessibility following PU.1 overexpression. The second (right) represents a SAHA-opened DHS site that does overlap PU.1 binding and exhibits a modest increase in accessibility following PU.1 overexpression