Transcriptome-wide identification of A > I RNA editing sites by inosine specific cleavage
Identifieur interne : 004507 ( Main/Merge ); précédent : 004506; suivant : 004508Transcriptome-wide identification of A > I RNA editing sites by inosine specific cleavage
Auteurs : Pierre B. Cattenoz [Australie, France] ; Ryan J. Taft [Australie] ; Eric Westhof [France] ; John S. Mattick [Australie]Source :
- 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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<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>
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