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. 2018 Jun 22;8:9536. doi: 10.1038/s41598-018-27919-8

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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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Model for Ajuba’s function during unperturbed S phase and replication stress (induced by HU treatment). (Left) During unperturbed S phase, Ajuba nuclear localization increases, and Ajuba associates with the RPA heterotrimer in the nucleus through direct interaction with RPA70- OB fold A. This interaction inhibits local ATR activation at the replication site. (Right) During replication stress (induced by HU treatment), Ajuba dissociates from RPA and allows for the assembly of the ATR-inducing complex. Ajuba is shuttled out of the nucleus via its NES (nuclear export signal). ATR activation takes place at the specific site of damage, but not at other sites in the genome where Ajuba continues to exert its repressive activity.