Editing Non-coding RNA (section)

===Prader–Willi syndrome===

The deletion of the 48 copies of the C/D box snoRNA [[Small nucleolar RNA SNORD116|SNORD116]] has been shown to be the primary cause of [[Prader&ndash;Willi syndrome]].<ref name="pmid18500341">{{cite journal | vauthors = Sahoo T, del Gaudio D, German JR, Shinawi M, Peters SU, Person RE, Garnica A, Cheung SW, Beaudet AL | display-authors = 6 | title = Prader-Willi phenotype caused by paternal deficiency for the HBII-85 C/D box small nucleolar RNA cluster | journal = Nature Genetics | volume = 40 | issue = 6 | pages = 719–721 | date = June 2008 | pmid = 18500341 | pmc = 2705197 | doi = 10.1038/ng.158 }}</ref><ref name="pmid18166085">{{cite journal | vauthors = Skryabin BV, Gubar LV, Seeger B, Pfeiffer J, Handel S, Robeck T, Karpova E, Rozhdestvensky TS, Brosius J | display-authors = 6 | title = Deletion of the MBII-85 snoRNA gene cluster in mice results in postnatal growth retardation | journal = PLOS Genetics | volume = 3 | issue = 12 | pages = e235 | date = December 2007 | pmid = 18166085 | pmc = 2323313 | doi = 10.1371/journal.pgen.0030235 | doi-access = free }}</ref><ref name="pmid18320030">{{cite journal | vauthors = Ding F, Li HH, Zhang S, Solomon NM, Camper SA, Cohen P, Francke U | title = SnoRNA Snord116 (Pwcr1/MBII-85) deletion causes growth deficiency and hyperphagia in mice | journal = PLOS ONE | volume = 3 | issue = 3 | pages = e1709 | date = March 2008 | pmid = 18320030 | pmc = 2248623 | doi = 10.1371/journal.pone.0001709 | veditors = Akbarian S | doi-access = free | bibcode = 2008PLoSO...3.1709D }}</ref><ref name="pmid16075369">{{cite journal | vauthors = Ding F, Prints Y, Dhar MS, Johnson DK, Garnacho-Montero C, Nicholls RD, Francke U | title = Lack of Pwcr1/MBII-85 snoRNA is critical for neonatal lethality in Prader-Willi syndrome mouse models | journal = Mammalian Genome | volume = 16 | issue = 6 | pages = 424–431 | date = June 2005 | pmid = 16075369 | doi = 10.1007/s00335-005-2460-2 | s2cid = 12256515 }}</ref> Prader–Willi is a developmental disorder associated with over-eating and learning difficulties. SNORD116 has potential target sites within a number of protein-coding genes, and could have a role in regulating alternative splicing.<ref name="pmid18160232">{{cite journal | vauthors = Bazeley PS, Shepelev V, Talebizadeh Z, Butler MG, Fedorova L, Filatov V, Fedorov A | title = snoTARGET shows that human orphan snoRNA targets locate close to alternative splice junctions | journal = Gene | volume = 408 | issue = 1–2 | pages = 172–179 | date = January 2008 | pmid = 18160232 | pmc = 6800007 | doi = 10.1016/j.gene.2007.10.037 }}</ref>