UMMS Affiliation

Program in Molecular Medicine; RNA Therapeutics Institute

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Biochemistry | Developmental Biology | Genetics | Genomics | Molecular Biology | Molecular Genetics


The double-stranded RNA-binding protein Staufen has been implicated in various post-transcriptional gene regulatory processes. Here we demonstrate that the Caenorhabditis elegans homolog of Staufen, STAU-1, functionally interacts with microRNAs. Loss-of-function mutations of stau-1 significantly suppress phenotypes of let-7 family microRNA mutants, a hypomorphic allele of dicer and a lsy-6 microRNA partial loss-of-function mutant. Furthermore, STAU-1 modulates the activity of lin-14, a target of lin-4 and let-7 family microRNAs, and this modulation is abolished when the 3' untranslated region of lin-14 is removed. Deep sequencing of small RNA cDNA libraries reveals no dramatic change in the levels of microRNAs, or other small RNA populations between wild type and stau-1 mutant, with the exception of certain endogenous siRNAs in the WAGO pathway. The modulation of microRNA activity by STAU-1 does not seem to be associated with the previously reported enhanced exogenous RNAi (Eri) phenotype of stau-1 mutants since eri-1 exhibits the opposite effect on microRNA activity. Altogether, our results suggest that STAU-1 negatively modulates microRNA activity downstream of biogenesis, possibly by competing with microRNAs for binding on the 3' untranslated region of target mRNAs.


microRNA, stau-1, RNAi, RNA-binding protein, 3’UTR

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Copyright © 2016 Author et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

DOI of Published Version



G3 (Bethesda). 2016 Feb 26. pii: g3.116.027300. doi: 10.1534/g3.116.027300. [Epub ahead of print]. Link to article on publisher's website

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G3 (Bethesda)


Early Online version of manuscript.

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Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.