Fig. 1: ATAC-seq data analysis in the amygdala of acute ethanol exposed rats.
From: Unraveling the epigenomic and transcriptomic interplay during alcohol-induced anxiolysis

A Heatmap showing differential ATAC peaks (FDR < 0.2; 345 peaks) and chromatin accessibility in the amygdala after acute ethanol exposure. Red represents increases in peaks and blue represents decreases in peaks. Individual peaks are represented in rows and individual animals from control and ethanol groups (n = 6 animal per treatment) are shown in columns. B Distribution of ATAC peak fold changes indicating that out of the 164 peaks at FDR < 0.05, 148 peaks were associated with ‘open’ chromatin regions in the amygdala of acute ethanol-treated compared to 16 peaks in the control rats. C ATAC-seq data analysis in the amygdala of acute ethanol exposed rats showing distribution of ATAC peaks across genomic features. D Footprinting images for the top 3 (out of 41) motifs derived from FIMO analysis of 572 vertebrate motifs from the JASPAR database. The motifs satisfied the following criteria: q < 0.01 and >50% enrichment (log2 ratio >0.585). The blue lines represent controls and the red lines represent ethanol-treated samples. [(NR3C1- Glucocorticoid Receptor; Nuclear Receptor Subfamily 3 Group C Member 1), (AR- Androgen Receptor), NR3C2 (Mineralocorticoid Receptor; Nuclear Receptor Subfamily 3 Group C Member 2)].