Abstract

C/D box snoRNAs (SNORDs) are an abundantly expressed class of short, non‐coding RNAs that have been long known to perform 2′‐O‐methylation of rRNAs. However, approximately half of human SNORDs have no predictable rRNA targets, and numerous SNORDs have been associated with diseases that show no defects in rRNAs, among them Prader‐Willi syndrome, Duplication 15q syndrome and cancer. This apparent discrepancy has been addressed by recent studies showing that SNORDs can act to regulate pre‐mRNA alternative splicing, mRNA abundance, activate enzymes, and be processed into shorter ncRNAs resembling miRNAs and piRNAs. Furthermore, recent biochemical studies have shown that a given SNORD can form both methylating and non‐methylating ribonucleoprotein complexes, providing an indication of the likely physical basis for such diverse new functions. Thus, SNORDs are more structurally and functionally diverse than previously thought, and their role in gene expression is under‐appreciated. The action of SNORDs in non‐methylating complexes can be substituted with oligonucleotides, allowing devising therapies for diseases like Prader‐Willi syndrome.

Document Type

Article

Publication Date

6-2017

Notes/Citation Information

Published in BioEssays, v. 39, issue 6, 1600264, p. 1-28.

© 2017 WILEY Periodicals, Inc.

The copyright holder has granted the permission for posting the article here.

This is the peer reviewed version of the following article: Falaleeva, M., Welden, J. R., Duncan, M. J., & Stamm, S. (2017). C/D‐box snoRNAs form methylating and non‐methylating ribonucleoprotein complexes: Old dogs show new tricks. BioEssays, 39(6), which has been published in final form at https://doi.org/10.1002/bies.201600264. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.

Digital Object Identifier (DOI)

https://doi.org/10.1002/bies.201600264

Funding Information

Supported by the NIH (R21HD080035, R21NS098186 and the Foundation for Prader-Willi Research).

Related Content

Supplementary material online.

bies201600264-sup-0001-suppfig-s1.docx (156 kB)
Supporting Figure S1.

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