KO of GATA2AS increases H3K27ac modification on GATA2AS/LRF sites. (A) Percent of KLF1 or LRF diffbinds genes associated with putative cis-regulatory element bound by GATA2AS (coupled), cobound with GATA2AS, or their overlap (coupled/cobound) predicted by GREAT (left). Schematic diagram for the model of coupled, cobound, and coupled/cobound (right). (B) MA plot showing differential H3K27ac sites upon KO of GATA2AS in HUDEP2 cells. (C) Distribution of H3K27ac diffbinds in the genome. (D) Heat map of GATA2AS peaks and H3K27ac ChIP-seq signal on the 2 sets (with or without LRF binding) of GATA2AS binding sites for control and GATA2AS KO cells. (E) Read density plot of H3K27ac ChIP-seq signal on GATA2AS/LRF binding peaks. (F) Motifs enriched in H3K27ac diffbinds were analyzed with HOMER. q-value for all motifs <0.05. (G) Heat maps showing ChIP-seq signal of YY1 from ENCODE and published LDB1 data33 on upregulated and downregulated H3K27ac sites.
