ArticlePloS one2012
AU-rich element-mediated mRNA decay can occur independently of the miRNA machinery in mouse embryonic fibroblasts and Drosophila S2-cells.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Connections between 3' end processing and DNA damage response: Ten years later.Wiley interdisciplinary reviews. RNA · 2020Review
- How miRs and mRNA deadenylases could post-transcriptionally regulate expression of tumor-promoting protein PLD.Advances in biological regulation · 2018Review
- PARN deadenylase is involved in miRNA-dependent degradation of TP53 mRNA in mammalian cells.Nucleic acids research · 2015Article
- Single-molecule modeling of mRNA degradation by miRNA: Lessons from data.BMC systems biology · 2015Article
- MixMir: microRNA motif discovery from gene expression data using mixed linear models.Nucleic acids research · 2014Article
- Article
- Multiple functions of tristetraprolin/TIS11 RNA-binding proteins in the regulation of mRNA biogenesis and degradation.Cellular and molecular life sciences : CMLS · 2013Review
- Post-transcriptional regulatory networks in immunity.Immunological reviews · 2013Review
- Tristetraprolin (TTP): interactions with mRNA and proteins, and current thoughts on mechanisms of action.Biochimica et biophysica actaReview
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AU-rich elements (AREs) are regulatory sequences located in the 3' untranslated region of many short-lived mRNAs. AREs are recognized by ARE-binding proteins and cause rapid mRNA degradation. Recent reports claimed that the function of AREs may be--at least in part--relayed through the miRNA pathway. We have revisited this hypothesis using dicer knock-out mouse embryonic fibroblasts and cultured Drosophila cells. In contrast to the published results, we find no evidence for a general requirement of the miRNA pathway in the function of AREs. Endogenous ier3 mRNA, which is known to contain a functional ARE, was degraded rapidly at indistinguishable rates in wild type and dicer knock-out mouse embryonic fibroblasts. In cultured Drosophila cells, both ARE-containing GFP reporter mRNAs and the endogenous cecA1 mRNA were resistant to depletion of the mi/siRNA factors dcr-1, dcr-2, ago1 and ago2. Furthermore, the Drosophila miRNA originally proposed to recognize AU-rich elements, miR-289, is not detectably expressed in flies or cultured S2 cells. Even our attempts to overexpress this miRNA from its genomic hairpin sequence failed. Thus, this sequence cannot serve as link between the miRNA and the AU-rich element mediated silencing pathways. Taken together, our studies in mammalian and Drosophila cells strongly argue that AREs can function independently of miRNAs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.