RNA editing by ADAR1 prevents MDA5 sensing of endogenous dsRNA as nonself

Author:

Liddicoat Brian J.12,Piskol Robert3,Chalk Alistair M.12,Ramaswami Gokul3,Higuchi Miyoko4,Hartner Jochen C.5,Li Jin Billy3,Seeburg Peter H.4,Walkley Carl R.12

Affiliation:

1. St. Vincent’s Institute of Medical Research, Fitzroy, Victoria 3065, Australia.

2. Department of Medicine, St. Vincent’s Hospital, University of Melbourne, Fitzroy, Victoria 3065, Australia.

3. Department of Genetics, Stanford University, Stanford, CA 94305, USA.

4. Department of Molecular Neurobiology, Max Planck Institute for Medical Research, 69120 Heidelberg, Germany.

5. Taconic Biosciences, 51063 Cologne, Germany.

Abstract

RNA editing helps identify cellular RNAs Adenosine bases in messenger RNA (mRNAs) can be enzymatically modified and changed into inosine bases. This RNA “editing” is mediated by adenosine deaminase acting on RNA (ADAR) enzymes. Liddicoat et al. show that the in vivo targets of the principal editing enzyme, ADAR1, are long double-stranded RNA (dsRNA) structures in noncoding portions of cellular mRNAs. ADAR1-directed editing of these cellular targets is critical to avoid activation of an immune response to dsRNA in the cytoplasm, because dsRNA is also a marker of viral infection. Science , this issue p. 1115

Funder

NIH

Ellison Medical Foundation

National Health and Medical Research Council (NHMRC)

Leukaemia Foundation

German Academic Exchange Service

Leukaemia Foundation Ph.D. scholarship

NHMRC Career Development

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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