SNORD115: SNORD115 and SNORD116 are snoRNAs that have been implicated in the pathogenesis of Prader-Willi syndrome and schizophrenia [PMC6937981]. SNORD115 is part of the UBE3A-ATS transcript, which also contains SNORD109B and extends to overlap the UBE3A gene [PMC4171697]. Other snoRNAs in this region include SNORD64, SNORD107, SNORD109A, and SNORD116 [PMC3137005]. A radiolabeled riboprobe was used to probe for SNORD115 and SNORD116 in Hg19 [PMC3656643]. PWS patients lack the locus 15q11.2–q13.1 that contains six snoRNAs, including SNORD107, SNORD64, and SNORD115 [PMC7140444]. While the role of spliced lncRNA 116HG has not been investigated, it is known that SNORD115 regulates alternate splicing of a serotonin receptor [PMC3792690]. Mouse models have shown that ectopic expression of SNORD115 in the choroid plexus leads to a double-stranded structure formation with 5-Ht2cr pre-mRNA [PMC8037846]. There are a total of 393 snoRNA sequences, including members of the multi-copy gene families such as SNOD113, SNOD114, SNO114, SNO114, SNO114, SNO114, SNO114, SNO114, SNO1134, and SNO1136 [PMC4914119]. Hypermethylation was found in regions on both SNOD115 and SNO1136 in affected individuals [PMC7522197]. Engineered expression of members of SNOD115 in brain tissues other than brain parenchyma has been reported [PMC9382696]. Moreover, aberrant expression of SNOD115 and SNO1136 was found in a subgroup of MM patients [PMC9413531]. In transgenic mice lacking SNOD115 expression, increased editing but no changes in splicing profile of 5ht2c pre-mRNA were initially found, but a later analysis revealed a higher proportion of short splice isoform in the hypothalamus [PMC5865145]. Five additional alternative splicing targets of SNOD115 were also identified [PMC8508363].