Fig. 4: Chromatin accessibility profiling of iPSC-derived astrocytes in response to treatment with EtOH, acamprosate or naltrexone.

A ATAC-seq was performed using iPSC-derived astrocytes (n = 3) with or without drug treatment i.e. EtOH (25 mM), acamprosate (5 µM) or naltrexone (30 nM) for 7 days. Peaks were clustered by K-means clustering. The numbers on the right indicate peak signal density. B Distribution of genomic features of genome-wide DNA accessible regions. C Venn diagram showing chromatin accessible regions that could be affected by EtOH, acamprosate and naltrexone individually, paired, or all three as determined by ATAC-seq (FDR < 0.05). D Motif discovery analyses were performed using differential ATAC-seq peaks (FDR < 0.05) for each drug treatment condition. IRF3 was the most significant transcription factor enriched in the differential peak regions across all three treatment conditions. E Motif discovery analyses were performed using differential peaks as determined by ATAC-seq (FDR < 0.05) and DEGs as determined by RNA-seq (FDR < 0.05) after each drug treatment condition. Up=increase in both chromatin accessibility and gene expression. Down=decrease in both chromatin accessibility and gene expression.