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. 2020 Jan 2;122(5):613–623. doi: 10.1038/s41416-019-0624-1

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Schematic model of the possible mechanisms of RNA-dependent DNA repair (RDDR). Repair is initiated in the same way as canonical double-stranded break (DSB) repair; however, at the point of the ubiquitylation cascade, an RNA production/processing step occurs, which produces DDRNAs. This DDRNA either takes the form of small RNA, which could hybridise to the broken DNA via the aid of helicases such as DDX1 and DHX9, or of a long RNA molecule, which could bridge the break by hybridising to the DNA via a RAD52-dependent strand invasion mechanism. Either the small RNA acts as a sequence-specific signal and allows propagation of canonical DSB repair pathways, or the long RNA molecule is used as a template for high-fidelity repair.