Postprandial DNase accessibility and H3K27 acetylation.

RNA-seq, DNase-seq, and H3K27Ac ChIP-seq from livers of mice euthanized at ZT14-unfed and ZT14-fed. (A and B) Fasn, Srebf1, Igfbp1, and Pck1 mRNA expression and nearby DNase accessibility and H3K27Ac. Yellow regions mark DNase-accessible regions associated with differentially regulated H3K27Ac. Arrows mark differentially regulated DNase accessibility. (C) Differential H3K27Ac at DHSs. Increased H3K27Ac is marked by red, and decreased H3K27Ac is marked by dark gray, FDR n = 3). (D) Tag density of H3K27Ac ChIP-seq and DNase-seq at DHSs associated with feeding-regulated H3K27Ac. Statistical significance is calculated using a Mann–Whitney–Wilcoxon test. ***p > 0.001. (E) Correlation between differentially regulated DNase accessibility and H3K27Ac. Regression analysis is calculated for the differentially regulated DHSs (rde) and all DHSs (rall) using Pearson correlation. (F) Cumulative distribution of DHSs associated with feeding-regulated H3K27Ac near TSSs of feeding–up-regulated genes. (G) Cumulative distribution of DHSs associated with feeding-regulated H3K27Ac near TSS of feeding–down-regulated genes. A Kolmogorov–Smirnov test was applied to test for differential distribution of DHSs associated with feeding-regulated H3K27Ac (gray and orange line) compared to DHSs associated with no change of H3K27Ac (broken line). Numerical values for panels C–G are available in S2 Data. Bed graphs in panels A and B are available at GEO: GSE119713. ChIP, chromatin immunoprecipitation; DHS, DNase hypersensitive site; FDR, false discovery rate; H3K27Ac, Histone 3 lysine 27 acetylation; TSS, transcription start site.