The host gene for one of the identified SE events, ELOVL7, was among the 20 genes common to both the human and rat studies. This event had the largest variance for the genetically imputed PSI (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${{{\hat{\mathrm \Psi }}}}$$\end{document}Ψ^), thereby incurring high statistical power for MR causality inference [32, 61]. The ELOVL7 skipped exon (ENSE00002079807) is in the 5’UTR (Fig. 3A) and it does not change the protein sequence. We found that the change of \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${{{\hat{\mathrm \Psi }}}}$$\end{document}Ψ^ for this SE (Fig. 3B) correlated with differential expression of ELOVL7 itself, and 249 other genes (FDR < 0.05, Fig. 3C and Supplementary Table S3). Another notable example for AUD relevance is the gene heat shock protein family A (Hsp70) member 6 (HSPA6), which encodes a splicing factor found to be significantly upregulated in human brain upon alcohol intake [12]. HSPA6 was identified as a downstream gene of the SE in ELOVL7 as well as the events in LINC00665 and NSUN4.
