Publication details
Mammalian DIS3L2 exoribonuclease targets the uridylated precursors of let-7 miRNAs
| Authors | |
|---|---|
| Year of publication | 2013 |
| Type | Article in Periodical |
| Magazine / Source | RNA |
| MU Faculty or unit | |
| Citation | |
| web | http://rnajournal.cshlp.org/content/early/2013/10/18/rna.040055.113.abstract |
| Doi | http://dx.doi.org/10.1261/rna.040055.113 |
| Field | Genetics and molecular biology |
| Keywords | DIS3L2; RNA degradation; RNA uridylation; let-7 miRNA |
| Attached files | |
| Description | 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 syndromeassociated 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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