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. 2018 Dec 17;9:5406. doi: 10.1038/s41467-018-07855-x

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© The Author(s) 2018

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 — DYNLL1 and the OD mediate a bivalent mode of 53BP1 oligomerization. 53BP1 localisation and function is dependent upon bivalent OD- and DYNLL1-mediated modes of oligomerization (top, left). OD-mediated oligomerization alone is sufficient for chromatin binding but results in severe DSB repair defects (top, right). DYNLL1-mediated oligomerization is also sufficient to support recruitment of 53BP1 to damage sites, but does not support DNA repair (bottom, left). Loss of both OD and DYNLL1-mediated modes of oligomerization eliminates 53BP1 recruitment to DNA damage sites and all associated repair functions (bottom, right)