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. 2020 Jun 23;11:3181. doi: 10.1038/s41467-020-16997-w

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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. 7 — After a DSB, the Rad9 oligomers assembled at the lesion limit: (i) the hyper-loading of recombination factors Rpa1, Rad52 and Rad52; (ii) the Sgs1-Top3-Rmi1 and Mph1 axes for the strand rejection, favouring long-lived D-loop and complex HR sub-pathways associated with CO (BIR, long-tract GC, eGC); (iii) the Sgs1-Dna2 axis for the long-range resection and single-strand-annealing (SSA) repair associated with deletions.