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. 2023 Feb 18;6:193. doi: 10.1038/s42003-023-04570-2

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© The Author(s) 2023

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. 8 — a Original viral RNP is recruited to the molecular pore located on the DMV surface by N binding to Ubl1 of Nsp3. b Two Ubl1 molecules of adjacent Nsp3s interact with N protein to disrupt the N-RNA binding. N protein successively dissociates from the RNP through the dynamic N-Nsp3 (Ubl1) interactions, leading to the delivery of gRNA into DMV. c Intact gRNA enters the DMV and serves as a template for viral RNA replication. Free N proteins are released into the cytosol. RNP ribonucleoprotein, DMV double-membrane vesicle, gRNA genomic RNA.