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The Key to Deobfuscation is Pattern of Life, not Overcoming Encryption
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      Association of N6-methyladenosine with viruses and related diseases

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          Abstract

          Background

          N6-methyladenosine (m6A) modification is the most prevalent internal modification of eukaryotic mRNA modulating gene expression. m6A modification is a dynamic reversible process regulated by three protein groups: methyltransferases (writers), demethylases (erasers), and m6A-binding proteins (readers). m6A modification is involved in all phases of RNA metabolism, including RNA folding, stability, splicing, nuclear exporting, translational modulation and degradation.

          Main body

          In recent years, numerous studies have reported that abnormal m6A modification causes aberrant expression of important viral genes. Herein, we review the role of m6A in viral lifecycle and its contribution to the pathogenesis of human diseases. Particularly, we focus on the viruses associated with human diseases such as HIV-1, IAV, HBV, HCV, EBV and many others.

          Conclusions

          A better understanding of m6A-virus relationship would provide new insights into the viral replication process and pathogenesis of human diseases caused by viruses. In addition, exploration of the role of m6A in disease-causing viruses will reveal novel approaches for the treatment of such diseases.

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          Most cited references31

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          Ythdc2 is an N6-methyladenosine binding protein that regulates mammalian spermatogenesis

          Yueshuai Guo, Chuan Sheng He, Bin Shen … (2017)
          N 6 -methyladenosine (m 6 A) is the most common internal modification in eukaryotic mRNA. It is dynamically installed and removed, and acts as a new layer of mRNA metabolism, regulating biological processes including stem cell pluripotency, cell differentiation, and energy homeostasis. m 6 A is recognized by selective binding proteins; YTHDF1 and YTHDF3 work in concert to affect the translation of m 6 A-containing mRNAs, YTHDF2 expedites mRNA decay, and YTHDC1 affects the nuclear processing of its targets. The biological function of YTHDC2, the final member of the YTH protein family, remains unknown. We report that YTHDC2 selectively binds m 6 A at its consensus motif. YTHDC2 enhances the translation efficiency of its targets and also decreases their mRNA abundance. Ythdc2 knockout mice are infertile; males have significantly smaller testes and females have significantly smaller ovaries compared to those of littermates. The germ cells of Ythdc2 knockout mice do not develop past the zygotene stage and accordingly, Ythdc2 is upregulated in the testes as meiosis begins. Thus, YTHDC2 is an m 6 A-binding protein that plays critical roles during spermatogenesis.
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            Cytoplasmic m6A reader YTHDF3 promotes mRNA translation

            Ang Li, Yu-Sheng Chen, Xiao-Li Ping … (2017)
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              N6-methyladenosine demethylase FTO targets pre-mRNAs and regulates alternative splicing and 3′-end processing

              Marek Bartosovic, Helena Covelo Molares, Pavlina Gregorova … (2017)
              Abstract N6-methyladenosine (m6A) is the most abundant base modification found in messenger RNAs (mRNAs). The discovery of FTO as the first m6A mRNA demethylase established the concept of reversible RNA modification. Here, we present a comprehensive transcriptome-wide analysis of RNA demethylation and uncover FTO as a potent regulator of nuclear mRNA processing events such as alternative splicing and 3΄ end mRNA processing. We show that FTO binds preferentially to pre-mRNAs in intronic regions, in the proximity of alternatively spliced (AS) exons and poly(A) sites. FTO knockout (KO) results in substantial changes in pre-mRNA splicing with prevalence of exon skipping events. The alternative splicing effects of FTO KO anti-correlate with METTL3 knockdown suggesting the involvement of m6A. Besides, deletion of intronic region that contains m6A-linked DRACH motifs partially rescues the FTO KO phenotype in a reporter system. All together, we demonstrate that the splicing effects of FTO are dependent on the catalytic activity in vivo and are mediated by m6A. Our results reveal for the first time the dynamic connection between FTO RNA binding and demethylation activity that influences several mRNA processing events.
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                Author and article information

                Contributors
                Wenzhao Cheng: wenzhao.cheng@hotmail.com
                Ruian Xu: ruianxu@hqu.edu.cn
                Journal
                Journal ID (nlm-ta): Virol J
                Journal ID (iso-abbrev): Virol. J
                Title: Virology Journal
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1743-422X
                Publication date (Electronic): 11 November 2019
                Publication date PMC-release: 11 November 2019
                Publication date Collection: 2019
                Volume: 16
                Electronic Location Identifier: 133
                Affiliations
                [1 ]ISNI 0000 0000 8895 903X, GRID grid.411404.4, Engineering Research Center of Molecular Medicine, Ministry of Education, , Huaqiao University, ; Xiamen, China
                [2 ]ISNI 0000 0000 8895 903X, GRID grid.411404.4, School of Medicine, , Huaqiao University, ; Xiamen, China
                [3 ]ISNI 0000 0004 1797 9307, GRID grid.256112.3, Stem Cell Laboratory, The Second Affiliated Hospital, , Fujian Medical University, ; Quanzhou, China
                [4 ]Fujian Provincial Key Laboratory of Molecular Medicine & Fujian Provincial Key Laboratory of Precision Medicine and Molecular Detection in Universities, Xiamen, China
                Article
                Publisher ID: 1236
                DOI: 10.1186/s12985-019-1236-3
                PMC ID: 6849232
                PubMed ID: 31711514
                SO-VID: 5a7b7ddd-dc7c-4380-8c8f-069b76b10eb9
                Copyright © © The Author(s). 2019
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 23 July 2019
                Date accepted : 3 October 2019
                Funding
                Funded by: the National Natural Science Foundation of China
                Award ID: 81271692
                Award Recipient :
                Funded by: the Ocean Antithrombotic Fibrinolytic Enzyme Gene Bank of Taiwan Strait
                Award ID: 2014FJPT08
                Award Recipient :
                Funded by: the Science and Technology Innovation Public Technology Service Platform of Function of Drugs and Food
                Award ID: 3502Z20141015
                Award Recipient :
                Funded by: Education Department of Fujian Province
                Award ID: JA14020
                Award Recipient :
                Funded by: Subsidized Project for Postgraduates’ Innovative Fund in Scientific Research of Huaqiao University
                Award ID: 17013071028
                Award Recipient :
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: n6-methyladenosine (m6a),methyltransferases,demethylases,m6a-binding proteins,viral diseases
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: n6-methyladenosine (m6a), methyltransferases, demethylases, m6a-binding proteins, viral diseases

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