This study demonstrates that expression of tomato leaf curl New Delhi virus CP confers effective resistance against tomato yellow leaf curl China virus (TYLCCNV), another prominent geminivirus, and uncovers a novel mechanism by which a viral effector antagonizes viral CP-mediated host resistance during mixed viral infections.
Abstract
Viral coat protein (CP)-mediated resistance represents an effective strategy that confers robust antiviral defense in plants. However, the functional relevance of this resistance mechanism during mixed infections by distinct viral species remains largely elusive. Mixed viral infections in agricultural crops frequently lead to exacerbated disease symptoms and substantial yield losses, posing a severe threat to global agricultural production. In this study, we demonstrate that expression of tomato leaf curl New Delhi virus (ToLCNDV) CP confers effective resistance against tomato yellow leaf curl China virus (TYLCCNV), another prominent geminivirus. Strikingly, the βC1 protein encoded by TYLCCNV betasatellite can fully counteract this CP-mediated resistance through direct interaction with ToLCNDV CP and promotion of its proteasome-dependent degradation. We further identified the residue Tyr110 of βC1 as essential for the interaction and subsequent CP degradation. Consequently, βC1-mediated suppression of CP resistance promotes efficient systemic infection of ToLCNDV DNA A. Collectively, our results uncover a novel mechanism by which a viral effector antagonizes viral CP-mediated host resistance during mixed viral infections, offering important insights into viral pathogenesis and the development of sustainable disease control strategies.
Pathogenesis-related protein 1 (PR1) serves as a canonical plant defense marker; however, its specific role in conferring resistance against insect herbivores has remained elusive. Here, we delineate a complete PR1-mediated defense pathway in rice. We show that the cysteine protease OsXCP2, in a catalytic residue-dependent manner, cleaves PR1a at the conserved CNYS motif to release the OsCAPE1 peptide, which subsequently activates broad-spectrum resistance against phloem-feeding insects. Insect herbivory induces the co-expression of OsXCP2 and OsPR1a specifically in the phloem. And loss-of-function osxcp2 mutants exhibit compromised resistance, underscoring the functional importance of this pathway in rice anti-herbivore defense. Strikingly, the glycoprotein (G) of the leafhopper-transmitted rhabdovirus rice stripe mosaic virus (RSMV) is secreted into the phloem during viruliferous insect feeding. Mechanistically, RSMV G employs a dual strategy to subvert this defense: it competitively binds the C-terminus of PR1a, thereby blocking OsXCP2-mediated cleavage, and simultaneously sequesters the liberated OsCAPE1 peptide. This concerted inhibition suppresses PR1-dependent resistance against insect feeding and consequently promotes viral transmission. In summary, our study identifies a novel PR1-activated anti-herbivore pathway in rice and reveals a sophisticated viral effector mechanism that antagonizes it to facilitate vector-borne viral transmission.
Jingya Zhao, Tong-Yu Liu, Yuexiao He et al.· Plant Communications· 0 citations
ABSTRACT Geminiviruses severely threaten global crop production. Tomato yellow leaf curl virus (TYLCV) encodes multifunctional effector C4, which participates in diverse biological processes and interacts with host proteins to facilitate infection. Despite extensive studies on geminiviral C4, how TYLCV C4 suppresses tomato immunity remains poorly characterized. In this study, we identified the tomato 14‐3‐3 protein SlTFT2 as a specific interaction partner of the TYLCV C4 protein. We demonstrated that SlTFT2 functions as a positive regulator of antiviral defence, as its silencing enhanced systemic viral infection, whereas its overexpression restricted infection. A critical serine residue at position 86 in C4 was essential for this interaction, and mutation of this residue (S86A or S86L) in TYLCV infectious clones significantly attenuated viral infectivity. Furthermore, C4, but not the S86A or S86L mutants, reduced the nuclear accumulation of SlTFT2. Collectively, our findings establish that the C4–SlTFT2 interaction is indispensable for TYLCV‐mediated immunosuppression. Moreover, C4 promotes successful TYLCV infection by reducing the nuclear accumulation of SlTFT2 through this interaction, revealing a novel mechanism by which the virus subverts host defence by targeting a 14‐3‐3 protein.
Geminiviruses employ sophisticated immune evasion strategies to incite devastating diseases, posing a significant threat to global agricultural security. A central tactic involves the subversion of chloroplast-mediated immunity via viral effectors. Here, we elucidate how the pathogenicity determinant βC1 from ageratum yellow vein China betasatellite (AYVCNB) hijacks this defense system by targeting the chloroplast-localized protein organellar single-stranded DNA-binding protein 1 (OSB1). Functionally, OSB1 acts as a positive regulator of immunity by stabilizing AGD2‐LIKE DEFENSE RESPONSE PROTEIN 1 (ALD1) and promoting pipecolic acid biosynthesis. We demonstrate that AYVCNB-encoded βC1 physically interacts with OSB1, triggering its ubiquitin-proteasome-dependent degradation and consequently abrogating the OSB1-ALD1 defense module. Parallel to this finding, our recent work revealed that βC1 from tomato yellow leaf curl China betasatellite re-localizes OSB1 from the chloroplast to the cytoplasm and promotes its degradation. These results collectively demonstrate that targeting the OSB1-ALD1 defense module represents a widespread and conserved geminivirus mechanism to subvert chloroplast immunity.
Zuxian Pan, Yuzhen Mei, Fangfang Li et al.· Phytopathology Research· 0 citations
Plant viral symptoms are not merely passive consequences of infection but can represent adaptive strategies for enhancing transmission. The molecular mechanisms and ecological consequences of such virus-induced symptoms, particularly in perennial crops such as kiwifruit, require exploration. Here, in field experiments, we discovered a kiwifruit infected with a novel virus, Actinidia yellow ringspot virus (AYRSpV), which exhibits severe yellowing symptoms and significantly increases the attractiveness of pollinating insects such as bees and aphids during the flowering season. Given that AYRSpV is pollen-transmissible, this visual manipulation may facilitate the pollinator-mediated spread of the virus. We further explored whether the AYRSpV coat protein (CP) is a key virulence determinant that interacts with and targets the chlorophyll metabolic enzyme magnesium protoporphyrin IX methyltransferase (ChlM) for degradation, leading to a significant reduction in chlorophyll content and systemic leaf yellowing. Knockout of kiwifruit ChlM recapitulated the yellowing phenotype and further enhanced plant susceptibility to AYRSpV. Our study elucidates a pathway whereby a viral CP protein directly disrupts chlorophyll biosynthesis to induce leaf yellowing. Furthermore, we reveal a strategy wherein the virus exploits this symptom as a visual signal to manipulate pollinator behavior, thus creating a ‘symptom-mediated transmission’ loop. These findings provide a comprehensive understanding of the molecular and ecological mechanisms driving the spread of an emerging kiwifruit virus.
Ruotong Wang, Jierou Li, Xiaoling Li et al.· Horticulture Research· 0 citations
Background Foot-and-mouth disease virus (FMDV) causes substantial economic losses in global livestock production; however, the key host factors supporting its early infection process remain poorly characterized. Methods In this study, we performed an unbiased genome-wide CRISPR/Cas9 knockout screening using porcine cells to screen and identify host factors involved in FMDV infection. Results We identified that the E3 ubiquitin ligase RNF24 supports efficient FMDV entry. RNF24 depletion inhibits viral entry and replication, whereas its overexpression enhances viral infectivity. Mechanistically, RNF24 preferentially promotes K27-linked non-degradative polyubiquitination of leupaxin (LPXN) at lysine 162, driving LPXN’s trafficking to the plasma membrane. At the membrane, LPXN assembles a ternary integrin-LPXN-VP1 complex that strengthens virus-receptor interactions and promotes viral adsorption and entry. Disruption of this ubiquitination event via the LPXN K162R mutation impairs complex formation and compromises viral entry. Conclusion Together, our study reveals a ubiquitin-dependent RNF24-LPXN regulatory axis that supports FMDV entry, highlights the role of non-degradative ubiquitination in viral pathogenesis, and proposes this interface as a potential target for antiviral intervention.
Jinyan Zhang, Hai-Long Liu, Jian Du et al.· Frontiers in Cell and Develo...· 0 citations
The results demonstrate the cutting-edge potential of CRISPR/Cas9 multiplex approaches as next-generation methods for designing sustainable resistance to multifaceted plant virus diseases and contribute to understanding of CRISPR-based antiviral response mechanisms.
Farwa Yaqub, Sidra Ashraf, Ahmed Al‐Harrasi et al.· Plant Protection· 0 citations
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