Requirement of the RNA-editing enzyme ADAR2 for normal physiology in mice

Marion Horsch, Peter H. Seeburg, Thure Adler, Juan Antonio Aguilar-Pimentel, Lore Becker, Julia Calzada-Wack, Lilian Garrett, Alexander Götz, Wolfgang Hans, Miyoko Higuchi, Sabine M. Hölter, Beatrix Naton, Cornelia Prehn, Oliver Puk, Ildikó Rácz, Birgit Rathkolb, Jan Rozman, Anja Schrewe, Jerzy Adamski, Dirk H. BuschIrene Esposito, Jochen Graw, Boris Ivandic, Martin Klingenspor, Thomas Klopstock, Martin Mempel, Markus Ollert, Holger Schulz, Eckhard Wolf, Wolfgang Wurst, Andreas Zimmer, Valérie Gailus-Durner, Helmut Fuchs, Martin Hrabě De Angelis, Johannes Beckersa

Research output: Contribution to journalArticleResearchpeer-review

78 Citations (Scopus)


ADAR2, an RNA editing enzyme that converts specific adenosines to inosines in certain pre-mRNAs, often leading to amino acid substitutions in the encoded proteins, is mainly expressed in brain. Of all ADAR2-mediated edits, a single one in the pre-mRNA of the AMPA receptor subunit GluA2 is essential for survival. Hence, early postnatal death of mice lacking ADAR2 is averted when the critical edit is engineered into both GluA2 encoding Gria2 alleles. Adar2 -/-/Gria2R/R mice display normal appearance and life span, but the general phenotypic effects of global lack of ADAR2 have remained unexplored. Here we have employed the Adar2-/-/Gria2R/R mouse line, and Gria2R/R mice as controls, to study the phenotypic consequences of loss of all ADAR2-mediated edits except the critical one in GluA2. Our extended phenotypic analysis covering ∼320 parameters identified significant changes related to absence of ADAR2 in behavior, hearing ability, allergy parameters and transcript profiles of brain.

Original languageEnglish
Pages (from-to)18614-18622
Number of pages9
JournalJournal of Biological Chemistry
Issue number21
Publication statusPublished - 27 May 2011
Externally publishedYes


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