(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, but some evidence indicates that long noncoding RNAs (lncRNAs) might be implicated. LncRNAs are noncoding RNA molecules >200 nucleotides in length which are capable of interacting with both short RNAs and proteins and thus may serve as a “screwdriver” for spliceosome. It was shown that lncRNA Gomafu affects the formation of spliceosomes and inhibits splicing factor SF110. Another lncRNA, MALAT1, interacts with serine/arginine splicing factors causing deregulation of splicing in a genome-wide fashion11,12. Data on splicing in AUD are very scanty. Alcohol intake was shown to be associated with a mis-splicing of specific genes such as AMPA receptors13 and GABA-B receptors14. Disruption of splicing on a somewhat broader scale was observed in the brain cortex of human fetuses exposed to alcohol15.
