Reversible ADP-ribosylation of RNA.


Journal

Nucleic acids research
ISSN: 1362-4962
Titre abrégé: Nucleic Acids Res
Pays: England
ID NLM: 0411011

Informations de publication

Date de publication:
20 06 2019
Historique:
accepted: 23 04 2019
revised: 10 04 2019
received: 01 12 2018
entrez: 20 6 2019
pubmed: 20 6 2019
medline: 4 12 2019
Statut: ppublish

Résumé

ADP-ribosylation is a reversible chemical modification catalysed by ADP-ribosyltransferases such as PARPs that utilize nicotinamide adenine dinucleotide (NAD+) as a cofactor to transfer monomer or polymers of ADP-ribose nucleotide onto macromolecular targets such as proteins and DNA. ADP-ribosylation plays an important role in several biological processes such as DNA repair, transcription, chromatin remodelling, host-virus interactions, cellular stress response and many more. Using biochemical methods we identify RNA as a novel target of reversible mono-ADP-ribosylation. We demonstrate that the human PARPs - PARP10, PARP11 and PARP15 as well as a highly diverged PARP homologue TRPT1, ADP-ribosylate phosphorylated ends of RNA. We further reveal that ADP-ribosylation of RNA mediated by PARP10 and TRPT1 can be efficiently reversed by several cellular ADP-ribosylhydrolases (PARG, TARG1, MACROD1, MACROD2 and ARH3), as well as by MACROD-like hydrolases from VEEV and SARS viruses. Finally, we show that TRPT1 and MACROD homologues in bacteria possess activities equivalent to the human proteins. Our data suggest that RNA ADP-ribosylation may represent a widespread and physiologically relevant form of reversible ADP-ribosylation signalling.

Identifiants

pubmed: 31216043
pii: 5480135
doi: 10.1093/nar/gkz305
pmc: PMC6582358
doi:

Substances chimiques

Chromatin 0
DNA, Single-Stranded 0
MACROD2 protein, human 0
Proto-Oncogene Proteins 0
NAD 0U46U6E8UK
Adenosine Diphosphate Ribose 20762-30-5
Adenosine Diphosphate 61D2G4IYVH
RNA 63231-63-0
ADP Ribose Transferases EC 2.4.2.-
PARP10 protein, human EC 2.4.2.30
Poly(ADP-ribose) Polymerases EC 2.4.2.30
Phosphotransferases (Alcohol Group Acceptor) EC 2.7.1.-
Trpt1 protein, mouse EC 2.7.1.-
Hydrolases EC 3.-
DNA Repair Enzymes EC 6.5.1.-

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

5658-5669

Subventions

Organisme : Wellcome Trust
ID : 101794
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 210634
Pays : United Kingdom
Organisme : NINDS NIH HHS
ID : R01 NS088629
Pays : United States
Organisme : Biotechnology and Biological Sciences Research Council
Pays : United Kingdom

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press on behalf of Nucleic Acids Research.

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Auteurs

Deeksha Munnur (D)

Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK.

Edward Bartlett (E)

Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK.

Petra Mikolčević (P)

Division of Molecular Biology, Ruđer Bošković Institute, Zagreb, Croatia.

Ilsa T Kirby (IT)

Program in Chemical Biology, Department of Physiology and Pharmacology, Oregon Health and Science University, Portland, OR 97239, USA.

Johannes Gregor Matthias Rack (JGM)

Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK.

Andreja Mikoč (A)

Division of Molecular Biology, Ruđer Bošković Institute, Zagreb, Croatia.

Michael S Cohen (MS)

Program in Chemical Biology, Department of Physiology and Pharmacology, Oregon Health and Science University, Portland, OR 97239, USA.

Ivan Ahel (I)

Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK.

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Classifications MeSH