These observations prompted us to address the question of whether H3K4me1 serves as a beacon to recruit PU.1 and collaborating transcription factors, and/or whether these factors are able to initiate the deposition of this mark. Using the PUER inducible system, we performed ChIP-Seq for H3K4me1 in PUER cells at 0, 1 and 24 h of tamoxifen treatment. Very little change in H3K4me1 signal was observed after 1 h (38 peaks gained), but a marked increase occurred at 3328 locations by 24 h (>4× tags, 15% of total H3K4me1 peaks present at 0 h). To evaluate the relationship between PU. 1 binding and H3K4me1, we selected a subset of 7428 highly induced PU.1 binding sites (>8-fold increase in tag count at 1 h) which exhibited less than 2 tags at 0 h. These binding sites could be classified into three groups, 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
