Nuclear coat protein drives a multifaceted tolerance program during Turnip crinkle virus infection

Nuclear coat protein drives a multifaceted tolerance program during Turnip crinkle virus infection | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Letter Nuclear coat protein drives a multifaceted tolerance program during Turnip crinkle virus infection Dana J. Rademacher, Braeden Kingsolver, Akashata Dawane, Jared P. May This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8695072/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Plant viruses must replicate yet maintain host tissue viability to sustain infection and transmission. We show that Turnip crinkle virus (TCV) uses nuclear localization of its coat protein (CP) to coordinate this balance. A nuclear-export mutant (TCVNES) retained core CP functions but causd attenuated symptoms and accumulated ~10-fold less than wild-type TCV. Transcriptomics and functional assays demonstrated that nuclear CP is required for large-scale host reprogramming, including SA accumulation and RBOH-dependent reactive oxygen species (ROS) production that promote TCV accumulation, as well as autophagy induction. Genetic loss of NADPH oxidase-derived ROS (rbohD rbohF) or autophagy (atg5-1) triggered rapid tissue collapse, necrosis, and convergent collapse-associated transcriptional responses following TCV infection. Nuclear CP consistently accelerated symptom onset in all backgrounds and exacerbated cell death and necrosis in rbohD rbohF and atg5-1. Nuclear CP is therefore responsible for early symptom development yet also required to activate ROS- and autophagy-dependent tolerance pathways. Biological sciences/Microbiology/Virology Biological sciences/Plant sciences/Plant stress responses/Biotic Full Text Additional Declarations There is NO Competing Interest. Supplementary Files SupplementaryTable7.xlsx Supplementary Table 7 SupplementaryTable6.xlsx Supplementary Table 6 SupplementaryTable2.xlsx Supplementary Table 2 SupplementaryTable9.docx Supplementary Table 9 SupplementaryTable8.xlsx Supplementary Table 8 SupplementaryTable5.xlsx Supplementary Table 5 SupplementaryTable1.xlsx Supplementary Table 1 SupplementaryTable4.xlsx Supplementary Table 4 SupplementaryTable3.xlsx Supplementary Table 3 Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8695072","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Letter","associatedPublications":[],"authors":[{"id":589775303,"identity":"e474e77d-7199-4390-9660-f7ca0a9b697a","order_by":0,"name":"Dana J. 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We show that Turnip crinkle virus (TCV) uses nuclear localization of its coat protein (CP) to coordinate this balance. A nuclear-export mutant (TCVNES) retained core CP functions but causd attenuated symptoms and accumulated ~10-fold less than wild-type TCV. Transcriptomics and functional assays demonstrated that nuclear CP is required for large-scale host reprogramming, including SA accumulation and RBOH-dependent reactive oxygen species (ROS) production that promote TCV accumulation, as well as autophagy induction. Genetic loss of NADPH oxidase-derived ROS (rbohD rbohF) or autophagy (atg5-1) triggered rapid tissue collapse, necrosis, and convergent collapse-associated transcriptional responses following TCV infection. Nuclear CP consistently accelerated symptom onset in all backgrounds and exacerbated cell death and necrosis in rbohD rbohF and atg5-1. 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