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. 2019 Nov 14;2:413. doi: 10.1038/s42003-019-0655-4

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© The Author(s) 2019

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. 6 — Model for the roles of RecN in DSB repair following DNA end resection. Briefly, RecN expression is stimulated by the SOS response, which is activated after loading of RecA onto ssDNA overhangs (step 1). A RecN multimer (more than or equal to a tetramer) is initially loaded onto ssDNA or dsDNA regions of the damaged strand via topological entrapment (step 2). Subsequently, RecN slides along the DNA and is prevented from disassociating by the RecA filament, resulting in accumulation of RecN molecules at ssDNA regions (step 3). Next, RecN bound to the ssDNA region topologically captures a homologous dsDNA molecule in an ATP-dependent manner (step 4). The resultant ssDNA–dsDNA tethering promotes RecA-mediated homologous pairing and strand exchange (step 5)