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TUT‐DIS3L2 is a mammalian surveillance pathway for aberrant structured non‐coding RNAs
Author(s) -
Ustianenko Dmytro,
Pasulka Josef,
Feketova Zuzana,
Bednarik Lukas,
Zigackova Dagmar,
Fortova Andrea,
Zavolan Mihaela,
Vanacova Stepanka
Publication year - 2016
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201694857
Subject(s) - biology , small nucleolar rna , rna , exoribonuclease , reverse transcriptase , long non coding rna , non coding rna , microbiology and biotechnology , pseudogene , microrna , genetics , computational biology , rnase p , gene , genome
Uridylation of various cellular RNA species at the 3′ end has been generally linked to RNA degradation. In mammals, uridylated pre‐let‐7 miRNAs and mRNAs are targeted by the 3′ to 5′ exoribonuclease DIS3L2. Mutations in DIS3L2 have been associated with Perlman syndrome and with Wilms tumor susceptibility. Using in vivo cross‐linking and immunoprecipitation (CLIP) method, we discovered the DIS3L2‐dependent cytoplasmic uridylome of human cells. We found a broad spectrum of uridylated RNAs including rRNAs, snRNAs, snoRNAs, tRNAs, vault, 7SL, Y RNAs, mRNAs, lncRNAs, and transcripts from pseudogenes. The unifying features of most of these identified RNAs are aberrant processing and the presence of stable secondary structures. Most importantly, we demonstrate that uridylation mediates DIS3L2 degradation of short RNA polymerase II‐derived RNAs. Our findings establish the role of DIS3L2 and oligouridylation as the cytoplasmic quality control for highly structured ncRNAs.