FOXA2 binding increases in diet-induced fatty liver. (A) Heatmap of results of FOXA2 ChIP-seq showing that binding increases in livers of mice on WD (6985 sites in ND, 12,765 in WD8, 9695 in WD12). (B) Western blot analysis of protein nuclear extracts from two control livers (ND) and three livers from mice on WD8 (left) and two control livers (ND) and three livers from mice on WD12 (right) with antibodies to FOXA2 and histone H3 (loading control). FOXA2 protein expression does not change in mice on WD8 and WD12; hence, changes in FOXA2 binding are independent of its expression. (C) Enrichr analysis of overrepresented pathways in sites bound by FOXA2 in ND, WD8, and WD12. (D) Scanning motif of positional weight matrices in the JASPAR and TRANSFAC databases in regions bound by FOXA2 in each condition by PscanChIP identified highly enriched forkhead consensus sites for FOXA2. (E) Lamin B1 ChIP-seq signal (RPKM) calculated in the overlap pf lamin B1 domains in ND with FOXA2-binding sites in WD12 decreases with diet and steatosis progression. (F) H3K9me3 ChIP-seq signal (RPKM) calculated in the overlap of lamin B1 domains in ND with FOXA2-binding sites in WD12 decreases only at WD12.