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      Recent advances in dynamic m 6A RNA modification

      review-article
      Author(s): 1 , 2 , 1 , 3 , 2 , 4
      Publication date (Electronic):
      Journal: Open Biology
      Publisher: The Royal Society
      Keywords: m6A, mRNA, methylation

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          Abstract

          The identification of m 6A demethylases and high-throughput sequencing analysis of methylated transcriptome corroborated m 6A RNA epigenetic modification as a dynamic regulation process, and reignited its investigation in the past few years. Many basic concepts of cytogenetics have been revolutionized by the growing understanding of the fundamental role of m 6A in RNA splicing, degradation and translation. In this review, we summarize typical features of methylated transcriptome in mammals, and highlight the ‘writers’, ‘erasers’ and ‘readers’ of m 6A RNA modification. Moreover, we emphasize recent advances of biological functions of m 6A and conceive the possible roles of m 6A in the regulation of immune response and related diseases.

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          The obesity-associated FTO gene encodes a 2-oxoglutarate-dependent nucleic acid demethylase.

          Thomas Gerken, Christophe A J Girard, Yi-Chun Tung … (2007)
          Variants in the FTO (fat mass and obesity associated) gene are associated with increased body mass index in humans. Here, we show by bioinformatics analysis that FTO shares sequence motifs with Fe(II)- and 2-oxoglutarate-dependent oxygenases. We find that recombinant murine Fto catalyzes the Fe(II)- and 2OG-dependent demethylation of 3-methylthymine in single-stranded DNA, with concomitant production of succinate, formaldehyde, and carbon dioxide. Consistent with a potential role in nucleic acid demethylation, Fto localizes to the nucleus in transfected cells. Studies of wild-type mice indicate that Fto messenger RNA (mRNA) is most abundant in the brain, particularly in hypothalamic nuclei governing energy balance, and that Fto mRNA levels in the arcuate nucleus are regulated by feeding and fasting. Studies can now be directed toward determining the physiologically relevant FTO substrate and how nucleic acid methylation status is linked to increased fat mass.
          Article 0 comments Cited 504 times – based on 0 reviews     Review now
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            Identification of methylated nucleosides in messenger RNA from Novikoff hepatoma cells.

            R Desrosiers, K Friderici, F Rottman (1974)
            The poly(A) tract found in eukaryotic mRNA was used to study methylation in mRNA obtained from Novikoff hepatoma cells. Methyl labeling of RNA was achieved with L-[methyl-(3)H]methionine under conditions that suppress radioactive incorporation into the purine ring. RNA that contains a poly(A) segment was obtained from polysomal RNA by chromatography on oligo(dT)-cellulose. Sucrose density gradient centrifugation of this RNA revealed a pattern expected for mRNA. The composition of the methyl-labeled nucleosides in the RNA was analyzed after complete enzymatic degradation to nucleosides. By use of DEAE-cellulose (borate) chromatography, which separates 2'-O-methylnucleosides from normal and base-methylated nucleosides, about 50% of the radioactivity was recovered in the 2'-O-methylnucleoside fraction and 50% in the base-methylnucleoside fraction. High-speed liquid chromatography (Aminex A-5) of the 2'-O-methylnucleoside fraction produced four peaks coincident with the four 2'-O-methylnucleoside standards. Analysis of the base-methylnucleoside fraction revealed a unique pattern. While ribosomal RNA and tRNA possessed complex base-methylnucleoside patterns, the distribution in mRNA was quite simple, consisting predominantly of N(6)-methyladenosine. These results demonstrate a unique distribution of methylated nucleosides in mRNA. By analogy to ribosomal RNA synthesis, the presence of methylnucleosides in mRNA may reflect a cellular mechanism for the selective processing of certain mRNA sequences.
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              Inactivation of the Fto gene protects from obesity.

              Julia Fischer, Linda Koch, Christian Emmerling … (2009)
              Several independent, genome-wide association studies have identified a strong correlation between body mass index and polymorphisms in the human FTO gene. Common variants in the first intron define a risk allele predisposing to obesity, with homozygotes for the risk allele weighing approximately 3 kilograms more than homozygotes for the low risk allele. Nevertheless, the functional role of FTO in energy homeostasis remains elusive. Here we show that the loss of Fto in mice leads to postnatal growth retardation and a significant reduction in adipose tissue and lean body mass. The leanness of Fto-deficient mice develops as a consequence of increased energy expenditure and systemic sympathetic activation, despite decreased spontaneous locomotor activity and relative hyperphagia. Taken together, these experiments provide, to our knowledge, the first direct demonstration that Fto is functionally involved in energy homeostasis by the control of energy expenditure.
              Article 0 comments Cited 337 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Open Biol
                Journal ID (iso-abbrev): Open Biol
                Journal ID (publisher-id): RSOB
                Journal ID (hwp): royopenbio
                Title: Open Biology
                Publisher: The Royal Society
                ISSN (Electronic): 2046-2441
                Publication date Collection: April 2016
                Publication date (Electronic): 13 April 2016
                Publication date PMC-release: 13 April 2016
                Volume: 6
                Issue: 4
                Electronic Location Identifier: 160003
                Affiliations
                [1 ]State Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University , Tianjin 300071, People's Republic of China
                [2 ]Department of Immunobiology, School of Medicine, Yale University , New Haven, CT 06520, USA
                [3 ]The First Affiliated Hospital, Biomedical Translational Research Institute, Guangdong Province Key Laboratory of Molecular Immunology and Antibody Engineering, Jinan University , Guangzhou 510632, People's Republic of China
                [4 ]Howard Hughes Medical Institute , Chevy Chase, MD 20815, USA
                Author notes
                [†]

                These authors contributed equally to this study.

                Author information
                http://orcid.org/0000-0003-3573-6803
                http://orcid.org/0000-0003-4461-0778
                Article
                Publisher ID: rsob160003
                DOI: 10.1098/rsob.160003
                PMC ID: 4852458
                PubMed ID: 27249342
                SO-VID: 8e588ff3-7ad2-4eed-9a5b-f099a2476635
                Copyright © © 2016 The Authors.
                License:

                Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.

                History
                Date received : 4 January 2016
                Date accepted : 18 March 2016
                Funding
                Funded by: Howard Hughes Medical Institute;
                Funded by: Key International Collaboration;
                Funded by: National Natural Science Foundation of China;
                Award ID: 31420103901
                Award ID: NIH T32 2T32DK007356
                Categories
                Subject: 1001
                Subject: 15
                Subject: 33
                Subject: Review
                Subject: Review Articles
                Custom metadata
                cover-date April 2016

                ScienceOpen disciplines: Life sciences
                Keywords: m6a,mrna,methylation
                Data availability:
                ScienceOpen disciplines: Life sciences
                Keywords: m6a, mrna, methylation

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