ArticlePlant physiology2024
Potato virus Y viral protein 6K1 inhibits the interaction between defense proteins during virus infection.
Article in Plant physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Tomato Yellow Leaf Curl Virus C4 Suppresses Antiviral Immunity by Targeting the 14-3-3 Protein SlTFT2.Molecular plant pathology · 2026Article
- Poplar miR1447 Is a Negative Regulator of Disease Resistance Through the SA-Dependent Pathway.Plant biotechnology journal · 2026Article
- Systematic Screening of Host Interactors forPlants (Basel, Switzerland) · 2026Article
- Characterization of the SoybeanPlants (Basel, Switzerland) · 2026Article
- Review
- High-Throughput Screening of Antiviral Agents Using the Fluorescence-Based Local Lesion Inspection Assay.Methods in molecular biology (Clifton, N.J.) · 2026Article
- G-Box Factors 14-3-3 Proteins Negatively RegulatePlants (Basel, Switzerland) · 2025Article
- Oligomeric SWEET1g of Solanum tuberosum confers resistance to potato virus Y and Potato virus X.The Plant journal : for cell and molecular biology · 2025Article
- A conserved lysine/arginine-rich motif is essential for the autophagic degradation of potyviral 6K1 protein and virus infection.Journal of virology · 2025Article
- The 6-kilodalton peptide 1 of the familyFrontiers in microbiology · 2025Review
- Integrative transcriptome and WGCNA analysis reveal key genes mainly in response toFrontiers in plant science · 2025Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
14-3-3 proteins play vital roles in plant defense against various pathogen invasions. To date, how 14-3-3 affects virus infections in plants remains largely unclear. In this study, we found that Nicotiana benthamiana 14-3-3h interacts with TRANSLATIONALLY CONTROLLED TUMOR PROTEIN (TCTP), a susceptibility factor of potato virus Y (PVY). Silencing of Nb14-3-3h facilitates PVY accumulation, whereas overexpression of Nb14-3-3h inhibits PVY replication. The antiviral activities of 3 Nb14-3-3h dimerization defective mutants are significantly decreased, indicating that dimerization of Nb14-3-3h is indispensable for restricting PVY infection. Our results also showed that the mutant Nb14-3-3hE16A, which is capable of dimerizing but not interacting with NbTCTP, has reduced anti-PVY activity; the mutant NbTCTPI65A, which is unable to interact with Nb14-3-3h, facilitates PVY replication compared with the wild-type NbTCTP, indicating that dimeric Nb14-3-3h restricts PVY infection by interacting with NbTCTP and preventing its proviral function. As a counter-defense, PVY 6K1 interferes with the interaction between Nb14-3-3h and NbTCTP by competitively binding to Nb14-3-3h and rescues NbTCTP to promote PVY infection. Our results provide insights into the arms race between plants and potyviruses.
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Registered trials
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