Mammalian DIS3L2 exoribonuclease targets the uridylated precursors of let-7 miRNAs

Investor logo
Investor logo
Investor logo
Investor logo

Warning

This publication doesn't include Faculty of Arts. It includes Central European Institute of Technology. Official publication website can be found on muni.cz.
Authors

USTIANENKO Dmytro HROŠŠOVÁ Dominika POTĚŠIL David CHALUPNÍKOVÁ Kateřina HRAZDILOVÁ Kristýna PACHERNÍK Jiří CETKOVSKÁ Kateřina ULDRIJAN Stjepan ZDRÁHAL Zbyněk VAŇÁČOVÁ Štěpánka

Year of publication 2013
Type Article in Periodical
Magazine / Source RNA
MU Faculty or unit

Central European Institute of Technology

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.
Related projects:

You are running an old browser version. We recommend updating your browser to its latest version.