Genome-wide patterns of heptad TF binding in fractionated primary human HSPCs. (A) Human MNCs were isolated from granulocyte-colony stimulating factor–stimulated donors or patients with a nonhematologic malignancy before being enriched for CD34 expression using magnetic-activated cell sorting (MACS) and further subfractionated into individual stem and progenitor cells based on surface marker expression using fluorescence-activated cell sorting (FACS) (colored cells are those studied in this manuscript). (B) The workflow and analysis pipeline followed for ChIPmentation and ChIP-seq experiments. (C) UCSC browser track at the RUNX1 locus (GRCh38 chr21:34,627,969-35,209,177) showing the reads per kilobase of transcript, per million mapped reads (RPKM)-normalized signal from FLI1, ERG, GATA2, RUNX1, TAL1, LYL1, and LMO2, along with H3K4me3, H3K27ac, H3K27me3, immunoglobulin G (IgG) (control), and publicly available RNA-seq tracks (GSE75384) for the 4 cell types. Full UCSC browser tracks are available http://genome.ucsc.edu/s/PimandaLab/Heptad_Regulome. (D) Characterization of identified peaks. Number of TF peaks were identified by macs2 (P value ≤ 1e−5) and their overall distribution along the genome (as percentages of total peaks identified) is shown. Each peak was assigned as either promoter-like (proximal [orange] or adjacent [blue], based on its distance from the TSS), intragenic [green], or intergenic [red], and enrichment (fraction of peaks containing that motif) calculated for the known ETS, GATA, RUNX, and E-Box motifs.