Abstract
The decapping scavenger enzyme DcpS is known for its role in hydrolyzing the cap structure following mRNA degradation. Recently, we discovered a new function in miRNA degradation activation for the ortholog of DcpS in C. elegans. Here we show that human DcpS conserves its role in miRNA turnover. In human cells, DcpS is a nucleocytoplasmic shuttling protein that activates miRNA degradation independently of its scavenger decapping activity in the cytoplasmic compartment. We also demonstrate that this new function for DcpS requires the contribution of the 5′-3′ exonuclease Xrn2. Our findings support a conserved role of DcpS as a modulator of miRNA turnover in animals.
Highlights
The decapping scavenger enzyme DcpS is known for its role in hydrolyzing the cap structure following mRNA degradation
In order to further confirm the direct implication of DcpS in miRNA degradation, we treated the cells with a compound that binds to the closed active site conformation of dimer DcpS and inhibits its activity[9]
Our observations demonstrate that the DcpS function in miRNA turnover originally observed in nematodes is conserved in human cells
Summary
The decapping scavenger enzyme DcpS is known for its role in hydrolyzing the cap structure following mRNA degradation. We discovered a new function in miRNA degradation activation for the ortholog of DcpS in C. elegans. DcpS is a nucleocytoplasmic shuttling protein that activates miRNA degradation independently of its scavenger decapping activity in the cytoplasmic compartment. The involvement of some ribonucleases in the degradation of specific mature miRNAs has been reported in plants (SDNs), Caenorhabditis elegans (XRN-1 and XRN-2), and human cells (Xrn[1], PNPase and RRP4)[7]. We have identified DCS-1, the ortholog of the human decapping scavenger enzyme DcpS, as a new modulator of miRNA turnover in Caenorhabditis elegans. We report that the cytoplasmic DcpS activates miRNAs degradation in human cells with the contribution of the 5′ -3′ exonuclease Xrn[2]. Our findings support a conserved role of DcpS as a modulator of miRNA turnover in animals
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