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Genes (Basel). 2017 Feb 11;8(2). pii: E68. doi: 10.3390/genes8020068.

Differential Binding of Three Major Human ADAR Isoforms to Coding and Long Non-Coding Transcripts.

Author information

1
Keio University Institute for Advanced Biosciences, Tsuruoka 997-0017, Japan. jgalipon@ttck.keio.ac.jp.
2
Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa 277-8562, Japan. rin-go2@jcom.home.ne.jp.
3
Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa 277-8562, Japan. ysuzuki@k.u-tokyo.ac.jp.
4
Keio University Institute for Advanced Biosciences, Tsuruoka 997-0017, Japan. mt@sfc.keio.ac.jp.
5
Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa 277-8562, Japan. ktei@bs.s.u-tokyo.ac.jp.
6
Graduate School of Science, The University of Tokyo, Tokyo 113-0032, Japan. ktei@bs.s.u-tokyo.ac.jp.

Abstract

RNA editing by deamination of adenosine to inosine is an evolutionarily conserved process involved in many cellular pathways, from alternative splicing to miRNA targeting. In humans, it is carried out by no less than three major adenosine deaminases acting on RNA (ADARs): ADAR1-p150, ADAR1-p110, and ADAR2. However, the first two derive from alternative splicing, so that it is currently impossible to delete ADAR1-p110 without also knocking out ADAR1-p150 expression. Furthermore, the expression levels of ADARs varies wildly among cell types, and no study has systematically explored the effect of each of these isoforms on the cell transcriptome. In this study, RNA immunoprecipitation (RIP)-sequencing on overexpressed ADAR isoforms tagged with green fluorescent protein (GFP) shows that each ADAR is associated with a specific set of differentially expressed genes, and that they each bind to distinct set of RNA targets. Our results show a good overlap with known edited transcripts, establishing RIP-seq as a valid method for the investigation of RNA editing biology.

KEYWORDS:

ADAR1-p110; ADAR1-p150; ADAR3; GO; KEGG; RIP sequence

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