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. 2018 Feb 15;8:3079. doi: 10.1038/s41598-018-21340-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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Hypothesis explaining the mechanism by which nuclear targeting of the RGNNV B1 protein via domains B and C induces p53/p21-mediated cell cycle arrest in GF-1 cells. The novel RGNNV non-structural protein B1 is expressed at an early replication stage (between 12 hpi and 24 hpi) in GF-1 cells. EYFP tagging shows the nuclear localization of B1 at 24 h (minor) and 48 hpi (mainly). Prediction of nuclear localization signals and domain deletion experiments showed that domains B and C, but not domains A and D, play a role in nuclear targeting. Nuclear targeting of the B1 protein induced cell cycle arrest of GF-1 cells at the G1/S phase via upregulation of p21 and p53 expression and downregulation of Cyclin D1, CDK4 and Mdm2 expression at 48 hpt.