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. 2020 Sep 24;11:4845. doi: 10.1038/s41467-020-18542-1

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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. 6 — a A model summarizing the function of the NLS-RXL/Cy module in infected cells. In the absence of Cyclin A (G0/G1, early), the NLS of M97 is functional and M97 is imported into the nucleus. MCMV induces Cyclin A and drives the cell cycle towards an S-phase environment (G1/S, late). Cyclin A binds to the RXL/Cy motif on M97 and masks the NLS, leading to cytosolic accumulation of M97–Cyclin A complexes. Cellular DNA synthesis is inhibited due to mislocalized Cyclin A. b Conservation of RXL/Cy-NLS modules across several cellular cell cycle regulatory proteins. The depicted sequences are of human origin.