期刊
RNA
卷 19, 期 12, 页码 1632-1638出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1261/rna.040055.113
关键词
DIS3L2; RNA degradation; RNA uridylation; let-7 miRNA
资金
- Wellcome Trust [084316/Z/07/Z]
- Czech Science Foundation [305/11/1095, P305/12/G034, P206-12-G151]
- CEITEC-Central European Institute of Technology from the European Regional Development Fund [CZ.1.05/1.1.00/02.0068]
- Wellcome Trust [084316/Z/07/Z] Funding Source: Wellcome Trust
The mechanisms of gene expression regulation by miRNAs have been extensively studied. However, the regulation of miRNA function and decay has long remained enigmatic. Only recently, 3' uridylation via LIN28A-TUT4/7 has been recognized as an essential component controlling the biogenesis of let-7 miRNAs in stem cells. Although uridylation has been generally implicated in miRNA degradation, the nuclease responsible has remained unknown. Here, we identify the Perlman syndrome-associated protein DIS3L2 as an oligo(U)-binding and processing exoribonuclease that specifically targets uridylated pre-let-7 in vivo. This study establishes DIS3L2 as the missing component of the LIN28-TUT4/7-DIS3L2 pathway required for the repression of let-7 in pluripotent cells.
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