Changes in gene expression may have manifold etiologies. One likely epigenetic precursor is the accessibility of chromatin, which exerts a cis-regulatory effect on gene expression. For example, a recent study using an assay for transposase-accessible chromatin with sequencing (ATAC-seq25) found differences in chromatin accessibility associated with chronic and acute alcohol exposure in the rat amygdala.26 However, AUD-associated linkages between open chromatin regions and gene expression are likely to be regionally and cell-type specific. The advent of single nucleus multiome experiments (sn-multiome), assaying both chromatin accessibility and gene expression within the same cell, provides remarkable opportunities to draw causal inferences regarding mechanisms underlying AUD-associated gene expression.
