In total, we found 713 differentially spliced genes in 740 clusters encompassing 5118 unique splicing events associated with AUD (see Fig. 3 and Supplementary File S4). Note, we identified more clusters than genes in these analyses as some genes had multiple clusters that were differentially spliced and because other clusters corresponded to a gene region without an official annotated gene symbol. Similar to previous analyses with these data, 92.3% of the reported differentially spliced genes associated with AUD7, were at least nominally significant in our analyses. We also identified exon skipping as the most frequent splicing event (53.9%) and found alternative splice donor events (4.0%) to be the least frequent. Differentially spliced genes were not enriched for gene ontological processes (all padj > 0.39), but several addiction genes were found to be differentially spliced, including ALDH3A2, CAMK2D, CAMKK2, GRIA2, GRK4, GRK6, HDAC3, PPP2R1B, and PRKACB (see Supplementary Figs. S3–S4). The GRIA2 gene showed differential splicing in a putative ‘flip flop’ splicing site (see Supplementary Fig. S5), which alters the rate of AMPA receptor opening38,39 and has been implicated with chronic
