Next, we asked which mechanism may be responsible for such genome-wide alcohol-induced alterations in the splicing landscape. Splicing is governed mainly by major (U2-dependent) spliceosome which removes ~99.5% of all introns and consists of five snRNAs and multiple proteins, known as splicing factors. Furthermore, there is a minor (U12-dependent) spliceosome that is responsible for splicing of atypical snU12-type introns that constitute only ~0.5% of all introns in the human genome (process, also known as noncanonical splicing)24. We set out to determine if alcohol affects the expression of snRNAs and splicing factors in SFC, NA, BLA, and CNA. We started with small nuclear RNAs (snRNAs), as they are involved in the recognition of introns, formation of splicing complexes, and splicing reactions. Although data on AUD-induced changes in splicing have begun to accumulate15, the impact of alcohol on snRNA in the brain is not elucidated. We initially studied the expression of canonical snRNAs transcripts: snU1, snU4, snU6, and snU7 (expression of other canonical snRNA transcripts such as snU2, snU4atac, snU6atac, snU11, and snU12 was not reliably detected in our RNA sequencing output).
