ADAR-mediated RNA editing of DNA:RNA hybrids is required for DNA double strand break repair

Sonia Jimeno (), Rosario Prados-Carvajal, María Jesús Fernández-Ávila, Sonia Silva, Domenico Alessandro Silvestris, Martín Endara-Coll, Guillermo Rodríguez-Real, Judit Domingo-Prim, Fernando Mejías-Navarro, Amador Romero-Franco, Silvia Jimeno-González, Sonia Barroso, Valeriana Cesarini, Andrés Aguilera, Angela Gallo, Neus Visa and Pablo Huertas ()
Additional contact information
Sonia Jimeno: Universidad de Sevilla
Rosario Prados-Carvajal: Universidad de Sevilla
María Jesús Fernández-Ávila: Centro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide
Sonia Silva: Universidad de Sevilla
Domenico Alessandro Silvestris: IRCCS Ospedale Pediatrico “Bambino Gesù”
Martín Endara-Coll: The Wenner-Gren Institute, Stockholm University
Guillermo Rodríguez-Real: Universidad de Sevilla
Judit Domingo-Prim: The Wenner-Gren Institute, Stockholm University
Fernando Mejías-Navarro: Universidad de Sevilla
Amador Romero-Franco: Universidad de Sevilla
Silvia Jimeno-González: Universidad de Sevilla
Sonia Barroso: Universidad de Sevilla
Valeriana Cesarini: IRCCS Ospedale Pediatrico “Bambino Gesù”
Andrés Aguilera: Universidad de Sevilla
Angela Gallo: IRCCS Ospedale Pediatrico “Bambino Gesù”
Neus Visa: The Wenner-Gren Institute, Stockholm University
Pablo Huertas: Universidad de Sevilla

Nature Communications, 2021, vol. 12, issue 1, 1-15

Abstract: Abstract The maintenance of genomic stability requires the coordination of multiple cellular tasks upon the appearance of DNA lesions. RNA editing, the post-transcriptional sequence alteration of RNA, has a profound effect on cell homeostasis, but its implication in the response to DNA damage was not previously explored. Here we show that, in response to DNA breaks, an overall change of the Adenosine-to-Inosine RNA editing is observed, a phenomenon we call the RNA Editing DAmage Response (REDAR). REDAR relies on the checkpoint kinase ATR and the recombination factor CtIP. Moreover, depletion of the RNA editing enzyme ADAR2 renders cells hypersensitive to genotoxic agents, increases genomic instability and hampers homologous recombination by impairing DNA resection. Such a role of ADAR2 in DNA repair goes beyond the recoding of specific transcripts, but depends on ADAR2 editing DNA:RNA hybrids to ease their dissolution.

Date: 2021
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DOI: 10.1038/s41467-021-25790-2

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