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      Quantifying the RNA cap epitranscriptome reveals novel caps in cellular and viral RNA

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          Abstract

          Chemical modification of transcripts with 5′ caps occurs in all organisms. Here, we report a systems-level mass spectrometry-based technique, CapQuant, for quantitative analysis of an organism's cap epitranscriptome. The method was piloted with 21 canonical caps—m 7GpppN, m 7GpppNm, GpppN, GpppNm, and m 2,2,7GpppG—and 5 ‘metabolite’ caps—NAD, FAD, UDP-Glc, UDP-GlcNAc, and dpCoA. Applying CapQuant to RNA from purified dengue virus, Escherichia coli, yeast, mouse tissues, and human cells, we discovered new cap structures in humans and mice (FAD, UDP-Glc, UDP-GlcNAc, and m 7Gpppm 6A), cell- and tissue-specific variations in cap methylation, and high proportions of caps lacking 2′- O-methylation (m 7Gpppm 6A in mammals, m 7GpppA in dengue virus). While substantial Dimroth-induced loss of m 1A and m 1Am arose with specific RNA processing conditions, human lymphoblast cells showed no detectable m 1A or m 1Am in caps. CapQuant accurately captured the preference for purine nucleotides at eukaryotic transcription start sites and the correlation between metabolite levels and metabolite caps.

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          Nutrient-sensitive mitochondrial NAD+ levels dictate cell survival.

          Hongying Yang, Tianle Yang, Joseph A. Baur … (2007)
          A major cause of cell death caused by genotoxic stress is thought to be due to the depletion of NAD(+) from the nucleus and the cytoplasm. Here we show that NAD(+) levels in mitochondria remain at physiological levels following genotoxic stress and can maintain cell viability even when nuclear and cytoplasmic pools of NAD(+) are depleted. Rodents fasted for 48 hr show increased levels of the NAD(+) biosynthetic enzyme Nampt and a concomitant increase in mitochondrial NAD(+). Increased Nampt provides protection against cell death and requires an intact mitochondrial NAD(+) salvage pathway as well as the mitochondrial NAD(+)-dependent deacetylases SIRT3 and SIRT4. We discuss the relevance of these findings to understanding how nutrition modulates physiology and to the evolution of apoptosis.
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            N6-Methyladenosine in Flaviviridae Viral RNA Genomes Regulates Infection

            Nandan Gokhale, Alexa McIntyre, Michael J McFadden … (2016)
            Summary The RNA modification N6-methyladenosine (m6A) post-transcriptionally regulates RNA function. The cellular machinery that controls m6A includes methyltransferases and demethylases that add or remove this modification, as well as m6A-binding YTHDF proteins that promote the translation or degradation of m6A-modified mRNA. We demonstrate that m6A modulates infection by hepatitis C virus (HCV). Depletion of m6A methyltransferases or an m6A demethylase, respectively, increases or decreases infectious HCV particle production. During HCV infection, YTHDF proteins relocalize to lipid droplets, sites of viral assembly, and their depletion increases infectious viral particles. We further mapped m6A sites across the HCV genome and determined that inactivating m6A in one viral genomic region increases viral titer without affecting RNA replication. Additional mapping of m6A on the RNA genomes of other Flaviviridae, including dengue, Zika, yellow fever, and West Nile virus, identifies conserved regions modified by m6A. Altogether, this work identifies m6A as a conserved regulatory mark across Flaviviridae genomes.
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              CAGE: cap analysis of gene expression.

              Rimantas Kodzius, Miki Kojima, Hiromi Nishiyori … (2006)
              Article 0 comments Cited 160 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Nucleic Acids Res
                Journal ID (iso-abbrev): Nucleic Acids Res
                Journal ID (publisher-id): nar
                Title: Nucleic Acids Research
                Publisher: Oxford University Press
                ISSN (Print): 0305-1048
                ISSN (Electronic): 1362-4962
                Publication date (Print): 18 November 2019
                Publication date (Electronic): 02 September 2019
                Publication date PMC-release: 02 September 2019
                Volume: 47
                Issue: 20
                Page: e130
                Affiliations
                [1 ] State Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, Inner Mongolia University , Hohhot, People's Republic of China
                [2 ] School of Life Sciences, Inner Mongolia University , Hohhot, People's Republic of China
                [3 ] Antimicrobial Resistance Interdisciplinary Research Group, Singapore-MIT Alliance for Research and Technology , Singapore
                [4 ] Lee Kong Chian School of Medicine, Nanyang Technological University , Singapore
                [5 ] NTU Institute of Health Technologies, Interdisciplinary Graduate Programme, Nanyang Technological University , Singapore
                [6 ] Shanghai Blueray Biopharma , Shanghai, People's Republic of China
                [7 ] Cancer Science Institute of Singapore , Singapore
                [8 ] School of Biological Sciences, Nanyang Technological University , Singapore
                [9 ] Department of Microbiology, National University of Singapore , Singapore
                [10 ] Department of Biology, Saint Louis University , St. Louis, MO, USA
                [11 ] Departments of Biochemistry & Molecular Biology and Pharmacology & Toxicology, and Sealy Center for Structural Biology & Molecular Biophysics, University of Texas Medical Branch , Galveston, TX, USA
                [12 ] Synthetic Biology Center, Departments of Biological Engineering and Electrical Engineering and Computer Science, Massachusetts Institute of Technology , Cambridge, MA, USA
                [13 ] Department of Pharmacology, Weill Medical College, Cornell University , New York, NY, USA
                [14 ] Dept. of Biological Engineering, Massachusetts Institute of Technology , Cambridge, MA, USA
                Author notes
                To whom correspondence should be addressed. Tel: +1 617 253 8017; Fax: +1 617 324 5280; Email: pcdedon@ 123456mit.edu
                Correspondence may also be addressed to Jin Wang. Tel: +86 471 499 2435; Fax: +86 471 499 2278; Email: jinwang@ 123456imu.edu.cn
                Author information
                http://orcid.org/0000-0002-3918-8923
                http://orcid.org/0000-0001-7637-7275
                Article
                Publisher ID: gkz751
                DOI: 10.1093/nar/gkz751
                PMC ID: 6847653
                PubMed ID: 31504804
                SO-VID: 11acb583-d767-4386-8594-85bc983a01f5
                Copyright © © The Author(s) 2019. Published by Oxford University Press on behalf of Nucleic Acids Research.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@ 123456oup.com

                History
                Date accepted : 23 August 2019
                Date revision received : 16 July 2019
                Date received : 07 April 2019
                Page count
                Pages: 16
                Funding
                Funded by: National Institutes of Health 10.13039/100000002
                Award ID: ES022858
                Award ID: CA186702
                Funded by: National Research Foundation of Singapore 10.13039/501100001381
                Funded by: Inner Mongolia University 10.13039/501100003850
                Funded by: Nanyang Presidential Graduate Scholarship
                Categories
                Subject: Methods Online

                ScienceOpen disciplines: Genetics
                Data availability:
                ScienceOpen disciplines: Genetics

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