Fig. 1: Chem-map reveals genomic binding sites for the BET bromodomain-targeting drug JQ1.

a, Chem-map workflow—in permeabilized cells, a precomplex of biotinylated small molecules (yellow) and antibiotin antibody (black) bind to the chromatin target (protein or DNA). Then a secondary antibody (purple) tethering of pA–Tn5 transposomes (light blue) was recruited to the drug binding sites. Addition of Mg²⁺ activates the transposomes and integrates adapters (green and orange) in the proximity of the drug-binding sites. After DNA purification, genomic fragments with adapters at both ends are enriched via PCR, which allows the genome-wide identification of drug-binding sites by next-generation sequencing. b, Chemical structure of biotinylated JQ1. c, Pairwise intersection of enriched peaks across five technical replicates (T1−T5) in a biological replicate (B1) of K562 cells. d, Venn diagram illustrating the overlap of high-confidence binding sites of JQ1 (Chem-map, red) and its protein target BRD4 (CUT&Tag, black) in K562 cells. e, Genome browser views of JQ1 Chem-map (red), biotin negative control (red) and BRD4 CUT&Tag (black) and its negative control without adding primary antibody (first Ab), compared to published JQ1 Click-Chem-seq (blue) and BRD4 ChIP–seq (purple) data at the CCND2 gene locus. Green and orange boxes highlight regions of respective close-up views. f, FRiP analysis comparing JQ1 Chem-map (Cm, n = 5), BRD4 CUT&Tag (C&T, n = 5), JQ1 Click-Chem-seq (Click-seq, different JQ1 derivatives JQ1-TCO and JQ1-PA, n = 1) and BRD4 ChIP–seq in K562 cells. g, Comparison of JQ1 Chem-map and published JQ1 Click-Chem-seq signal averaged at highest-confidence loci detected with BRD4 CUT&Tag in K562 cells. All sequencing data are normalized by sequencing depth.