The finding that PU.1 binding leads to deposition of the H3K4me1 mark at promoter-distal sites that are correlated with cell type-specific patterns of gene expression (Heintzman et al., 2009) provides the initial evidence that PU.1 contributes to the ‘writing’ of this epigenetic signature on a genome-wide scale. Our data also indicate that PU.1 binding and nucleosome remodelling are not sufficient to result in the deposition of this mark in all cases (Figure 4C, Group III), suggesting that the mechanisms that ultimately lead to H3K4 monomethylation also require collaborative interactions with other transcription factors, such as C/EBPβ. Additionally, the motifs enriched in focally H3K4me1-marked promoter-distal regions in macrophages and B cells and the shape of the H3K4me1 patterns around the binding sites of three of these factors (C/EBPα/β, Oct-2) suggest that the other H3K4me1-associated factors are also involved in nucleosome displacement and targeting of H3K4me1 deposition around their binding sites. The observation that H3K4me1-marked regions in other tissues and cell types, including liver, erythrocytes, T cells and ES cells, also exhibit enrichment for limited sets of motifs for corresponding lineage determining
