Transcriptome-wide identification of A > I RNA editing sites by inosine specific cleavage
Identifieur interne : 001C27 ( Pmc/Corpus ); précédent : 001C26; suivant : 001C28Transcriptome-wide identification of A > I RNA editing sites by inosine specific cleavage
Auteurs : Pierre B. Cattenoz ; Ryan J. Taft ; Eric Westhof ; John S. MattickSource :
- RNA [ 1355-8382 ] ; 2013.
Abstract
Adenosine to inosine (A > I) RNA editing, which is catalyzed by the ADAR family of proteins, is one of the fundamental mechanisms by which transcriptomic diversity is generated. Indeed, a number of genome-wide analyses have shown that A > I editing is not limited to a few mRNAs, as originally thought, but occurs widely across the transcriptome, especially in the brain. Importantly, there is increasing evidence that A > I editing is essential for animal development and nervous system function. To more efficiently characterize the complete catalog of ADAR events in the mammalian transcriptome the authors developed a high-throughput protocol to identify A > I editing sites, which exploits the capacity of glyoxal to protect guanosine, but not inosine, from RNAse T1 treatment. Using this method they identified 665 editing sites in mouse brain RNA, including most known sites and suite of novel sites that include nonsynonymous changes to protein-coding genes and hyperediting of genes known to regulate p53.
Url:
DOI: 10.1261/rna.036202.112
PubMed: 23264566
PubMed Central: 3543087
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PMC:3543087Le document en format XML
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Taft</name><affiliation><nlm:aff id="af1">Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia</nlm:aff></affiliation></author><author><name sortKey="Westhof, Eric" sort="Westhof, Eric" uniqKey="Westhof E" first="Eric" last="Westhof">Eric Westhof</name><affiliation><nlm:aff id="af2">Architecture et Réactivité de l’ARN, Université de Strasbourg, Institut de biologie moléculaire et cellulaire du CNRS, 67084 Strasbourg Cedex, France</nlm:aff></affiliation></author><author><name sortKey="Mattick, John S" sort="Mattick, John S" uniqKey="Mattick J" first="John S." last="Mattick">John S. Mattick</name><affiliation><nlm:aff id="af1">Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia</nlm:aff></affiliation><affiliation><nlm:aff id="af3">Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">23264566</idno><idno type="pmc">3543087</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3543087</idno><idno type="RBID">PMC:3543087</idno><idno type="doi">10.1261/rna.036202.112</idno><date when="2013">2013</date><idno type="wicri:Area/Pmc/Corpus">001C27</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001C27</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Transcriptome-wide identification of A > I RNA editing sites by inosine specific cleavage</title><author><name sortKey="Cattenoz, Pierre B" sort="Cattenoz, Pierre B" uniqKey="Cattenoz P" first="Pierre B." last="Cattenoz">Pierre B. Cattenoz</name><affiliation><nlm:aff id="af1">Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia</nlm:aff></affiliation><affiliation><nlm:aff id="af2">Architecture et Réactivité de l’ARN, Université de Strasbourg, Institut de biologie moléculaire et cellulaire du CNRS, 67084 Strasbourg Cedex, France</nlm:aff></affiliation></author><author><name sortKey="Taft, Ryan J" sort="Taft, Ryan J" uniqKey="Taft R" first="Ryan J." last="Taft">Ryan J. Taft</name><affiliation><nlm:aff id="af1">Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia</nlm:aff></affiliation></author><author><name sortKey="Westhof, Eric" sort="Westhof, Eric" uniqKey="Westhof E" first="Eric" last="Westhof">Eric Westhof</name><affiliation><nlm:aff id="af2">Architecture et Réactivité de l’ARN, Université de Strasbourg, Institut de biologie moléculaire et cellulaire du CNRS, 67084 Strasbourg Cedex, France</nlm:aff></affiliation></author><author><name sortKey="Mattick, John S" sort="Mattick, John S" uniqKey="Mattick J" first="John S." last="Mattick">John S. Mattick</name><affiliation><nlm:aff id="af1">Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia</nlm:aff></affiliation><affiliation><nlm:aff id="af3">Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia</nlm:aff></affiliation></author></analytic><series><title level="j">RNA</title><idno type="ISSN">1355-8382</idno><idno type="eISSN">1469-9001</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Adenosine to inosine (A > I) RNA editing, which is catalyzed by the ADAR family of proteins, is one of the fundamental mechanisms by which transcriptomic diversity is generated. Indeed, a number of genome-wide analyses have shown that A > I editing is not limited to a few mRNAs, as originally thought, but occurs widely across the transcriptome, especially in the brain. Importantly, there is increasing evidence that A > I editing is essential for animal development and nervous system function. To more efficiently characterize the complete catalog of ADAR events in the mammalian transcriptome the authors developed a high-throughput protocol to identify A > I editing sites, which exploits the capacity of glyoxal to protect guanosine, but not inosine, from RNAse T1 treatment. Using this method they identified 665 editing sites in mouse brain RNA, including most known sites and suite of novel sites that include nonsynonymous changes to protein-coding genes and hyperediting of genes known to regulate p53.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">RNA</journal-id><journal-id journal-id-type="iso-abbrev">RNA</journal-id><journal-id journal-id-type="publisher-id">RNA</journal-id><journal-title-group><journal-title>RNA</journal-title></journal-title-group><issn pub-type="ppub">1355-8382</issn><issn pub-type="epub">1469-9001</issn><publisher><publisher-name>Cold Spring Harbor Laboratory Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">23264566</article-id><article-id pub-id-type="pmc">3543087</article-id><article-id pub-id-type="medline">9509184</article-id><article-id pub-id-type="publisher-id">RA</article-id><article-id pub-id-type="doi">10.1261/rna.036202.112</article-id><article-categories><subj-group subj-group-type="heading"><subject>Methods</subject></subj-group></article-categories><title-group><article-title>Transcriptome-wide identification of A > I RNA editing sites by inosine specific cleavage</article-title><alt-title alt-title-type="left-running">Cattenoz et al.</alt-title><alt-title alt-title-type="right-running">Characterization of A > I RNA editing by iSeq</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Cattenoz</surname><given-names>Pierre B.</given-names></name><xref ref-type="aff" rid="af1">1</xref><xref ref-type="aff" rid="af2">2</xref></contrib><contrib contrib-type="author"><name><surname>Taft</surname><given-names>Ryan J.</given-names></name><xref ref-type="aff" rid="af1">1</xref></contrib><contrib contrib-type="author"><name><surname>Westhof</surname><given-names>Eric</given-names></name><xref ref-type="aff" rid="af2">2</xref></contrib><contrib contrib-type="author"><name><surname>Mattick</surname><given-names>John S.</given-names></name><xref ref-type="aff" rid="af1">1</xref><xref ref-type="aff" rid="af3">3</xref><xref ref-type="corresp" rid="cor1">4</xref></contrib></contrib-group><aff id="af1"><label>1</label>Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia</aff><aff id="af2"><label>2</label>Architecture et Réactivité de l’ARN, Université de Strasbourg, Institut de biologie moléculaire et cellulaire du CNRS, 67084 Strasbourg Cedex, France</aff><aff id="af3"><label>3</label>Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia</aff><author-notes><corresp id="cor1"><label>4</label><bold>Corresponding author</bold><bold>E-mail <email xlink:type="simple">j.mattick@garvan.org.au</email></bold></corresp></author-notes><pub-date pub-type="ppub"><month>2</month><year>2013</year></pub-date><volume>19</volume><issue>2</issue><fpage>257</fpage><lpage>270</lpage><history><date date-type="received"><day>30</day><month>8</month><year>2012</year></date><date date-type="accepted"><day>14</day><month>11</month><year>2012</year></date></history><permissions><copyright-statement>Copyright © 2013 RNA Society</copyright-statement><copyright-year>2013</copyright-year></permissions><self-uri content-type="pdf" xlink:type="simple" xlink:href="257.pdf"></self-uri><abstract abstract-type="precis"><p>Adenosine to inosine (A > I) RNA editing, which is catalyzed by the ADAR family of proteins, is one of the fundamental mechanisms by which transcriptomic diversity is generated. Indeed, a number of genome-wide analyses have shown that A > I editing is not limited to a few mRNAs, as originally thought, but occurs widely across the transcriptome, especially in the brain. Importantly, there is increasing evidence that A > I editing is essential for animal development and nervous system function. To more efficiently characterize the complete catalog of ADAR events in the mammalian transcriptome the authors developed a high-throughput protocol to identify A > I editing sites, which exploits the capacity of glyoxal to protect guanosine, but not inosine, from RNAse T1 treatment. Using this method they identified 665 editing sites in mouse brain RNA, including most known sites and suite of novel sites that include nonsynonymous changes to protein-coding genes and hyperediting of genes known to regulate p53.</p></abstract><abstract><p>Adenosine to inosine (A > I) RNA editing, which is catalyzed by the ADAR family of proteins, is one of the fundamental mechanisms by which transcriptomic diversity is generated. Indeed, a number of genome-wide analyses have shown that A > I editing is not limited to a few mRNAs, as originally thought, but occurs widely across the transcriptome, especially in the brain. Importantly, there is increasing evidence that A > I editing is essential for animal development and nervous system function. To more efficiently characterize the complete catalog of ADAR events in the mammalian transcriptome we developed a high-throughput protocol to identify A > I editing sites, which exploits the capacity of glyoxal to protect guanosine, but not inosine, from RNAse T1 treatment, thus facilitating extraction of RNA fragments with inosine bases at their termini for high-throughput sequencing. Using this method we identified 665 editing sites in mouse brain RNA, including most known sites and suite of novel sites that include nonsynonymous changes to protein-coding genes, hyperediting of genes known to regulate p53, and alterations to non-protein-coding RNAs. This method is applicable to any biological system for the de novo discovery of A > I editing sites, and avoids the complicated informatic and practical issues associated with editing site identification using traditional RNA sequencing data. This approach has the potential to substantially increase our understanding of the extent and function of RNA editing, and thereby to shed light on the role of transcriptional plasticity in evolution, development, and cognition.</p></abstract><kwd-group><kwd>ADAR</kwd><kwd>noncoding RNA</kwd><kwd>ion channel</kwd><kwd>deep sequencing</kwd><kwd>genomics</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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