Post-transcriptional effects of alcohol are much less studied. Splicing is a nuclear post-transcriptional process of removing introns from pre-mRNA after which mature mRNA is produced and exported into the cytoplasm for translation (constitutive splicing). Alternative splicing is the process of selective incorporation of exons in mature mRNA transcripts which is responsible for transcriptomic and proteomic diversity. Perturbed splicing is implicated in a growing number of human diseases, including those related to the central nervous system. For example, cryptic splice site usage resulting in exon 7 skipping of PINK1 causes early-onset Parkinson’s disease, while increased inclusion of exon 10 in MAPT causes frontotemporal dementia with parkinsonism. Mechanistically, splicing is mediated by major and minor spliceosomes, nuclear machineries, each consisting of five small nuclear RNAs and dozens of splicing factors. Major spliceosome (also known as U2-dependent spliceosome) is composed of snRNAs U1 (snU1), snU2, snU4, snU5, and snU6 and is responsible for removal of ~99.5% introns. Minor spliceosome (also known as U12-dependent spliceosome) contains snU4atac, snU5, snU6atac, snU11, and snU12 and processes ~0.5% introns. Regulation of splicing and spliceosomes is poorly understood,
