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      Combinatorial Control of mRNA Fates by RNA-Binding Proteins and Non-Coding RNAs

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          Abstract

          Post-transcriptional control of gene expression is mediated by RNA-binding proteins (RBPs) and small non-coding RNAs (e.g., microRNAs) that bind to distinct elements in their mRNA targets. Here, we review recent examples describing the synergistic and/or antagonistic effects mediated by RBPs and miRNAs to determine the localisation, stability and translation of mRNAs in mammalian cells. From these studies, it is becoming increasingly apparent that dynamic rearrangements of RNA-protein complexes could have profound implications in human cancer, in synaptic plasticity, and in cellular differentiation.

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          RNA regulons: coordination of post-transcriptional events.

          Jack Keene (2007)
          Recent findings demonstrate that multiple mRNAs are co-regulated by one or more sequence-specific RNA-binding proteins that orchestrate their splicing, export, stability, localization and translation. These and other observations have given rise to a model in which mRNAs that encode functionally related proteins are coordinately regulated during cell growth and differentiation as post-transcriptional RNA operons or regulons, through a ribonucleoprotein-driven mechanism. Here I describe several recently discovered examples of RNA operons in budding yeast, fruitfly and mammalian cells, and their potential importance in processes such as immune response, oxidative metabolism, stress response, circadian rhythms and disease. I close by considering the evolutionary wiring and rewiring of these combinatorial post-transcriptional gene-expression networks.
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            RNA and disease.

            Thomas Cooper, Lili Wan, Gideon Dreyfuss (2009)
            Cellular functions depend on numerous protein-coding and noncoding RNAs and the RNA-binding proteins associated with them, which form ribonucleoprotein complexes (RNPs). Mutations that disrupt either the RNA or protein components of RNPs or the factors required for their assembly can be deleterious. Alternative splicing provides cells with an exquisite capacity to fine-tune their transcriptome and proteome in response to cues. Splicing depends on a complex code, numerous RNA-binding proteins, and an enormously intricate network of interactions among them, increasing the opportunity for exposure to mutations and misregulation that cause disease. The discovery of disease-causing mutations in RNAs is yielding a wealth of new therapeutic targets, and the growing understanding of RNA biology and chemistry is providing new RNA-based tools for developing therapeutics.
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              Relief of microRNA-mediated translational repression in human cells subjected to stress.

              Suvendra Bhattacharyya, Regula Habermacher, Ursula Martine … (2006)
              In metazoans, most microRNAs imperfectly base-pair with the 3' untranslated region (3'UTR) of target mRNAs and prevent protein accumulation by either repressing translation or inducing mRNA degradation. Examples of specific mRNAs undergoing microRNA-mediated repression are numerous, but whether the repression is a reversible process remains largely unknown. Here we show that cationic amino acid transporter 1 (CAT-1) mRNA and reporters bearing its 3'UTR can be relieved from the microRNA miR-122-induced inhibition in human hepatocarcinoma cells subjected to different stress conditions. The derepression of CAT-1 mRNA is accompanied by its release from cytoplasmic processing bodies and its recruitment to polysomes. The derepression requires binding of HuR, an AU-rich-element binding protein, to the 3'UTR of CAT-1 mRNA. We propose that proteins interacting with the 3'UTR will generally act as modifiers altering the potential of miRNAs to repress gene expression.
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                Author and article information

                Contributors
                Jürg Bähler: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Biomolecules
                Journal ID (iso-abbrev): Biomolecules
                Journal ID (publisher-id): biomolecules
                Title: Biomolecules
                Publisher: MDPI
                ISSN (Electronic): 2218-273X
                Publication date (Electronic): 24 September 2015
                Publication date Collection: December 2015
                Volume: 5
                Issue: 4
                Pages: 2207-2222
                Affiliations
                Department of Microbial & Cellular Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK; E-Mail: v.iadevaia@ 123456surrey.ac.uk
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: a.gerber@ 123456surrey.ac.uk ; Tel.: +44-1483-682-158; Fax: +44-1483-686-401.
                Article
                Publisher ID: biomolecules-05-02207
                DOI: 10.3390/biom5042207
                PMC ID: 4693235
                PubMed ID: 26404389
                SO-VID: 4392e1c1-a829-4802-935f-6828c8f5b91c
                Copyright © © 2015 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 17 July 2015
                Date accepted : 08 September 2015
                Categories
                Subject: Review

                Keywords: gene expression,post-transcriptional control,rna-binding protein,microrna,ribonucleoprotein complex,combinatorial control
                Data availability:
                Keywords: gene expression, post-transcriptional control, rna-binding protein, microrna, ribonucleoprotein complex, combinatorial control

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