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Yi-Xuan Wang

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Jul 2026

GLRaV-2 p24 suppressor simultaneously subverts host RNA silencing and SA defenses by targeting VvWRKY51.

Grapevine (Vitis vinifera) is severely impacted by viral diseases, with grapevine leafroll disease (GLRD) being the most economically damaging. Grapevine leafroll-associated virus 2 (GLRaV-2) is a prevalent virus associated with GLRD, yet the molecular mechanisms underlying GLRaV-2 infection remain poorly understood. Here, we demonstrate that the grapevine transcription factor (TF) VvWRKY51 ‌positively autoregulates its transcription‌ and ‌directly represses‌ salicylic acid (SA)-responsive defense genes VvPR1 (pathogenesis-related gene 1), VvPR2, and VvPR5. Through in vivo and in vitro assays, we demonstrate that GLRaV-2 RNA silencing suppressor p24 specifically interacts with VvWRKY51 to promote viral infection. p24 hijacks nuclear VvWRKY51 by translocating it to the cytoplasm, thereby enhancing its RNA silencing suppression activity via two mechanisms: (a) evading host degradation pathways (ubiquitin-proteasome system and autophagy), and (b) strengthening its siRNA-binding affinity. Concurrently, cytoplasmic p24 enters the nucleus by binding VvWRKY51, where it reinforces VvWRKY51-mediated transcriptional repression of VvPR1, VvPR2, and VvPR5. This occurs by enhancing VvWRKY51 binding to its own promoter and those of VvPR genes. Our findings reveal a novel viral strategy wherein a single viral suppressor of RNA silencing (VSR) simultaneously suppresses RNA silencing and SA-mediated immunity by interacting with a host TF to establish a permissive environment for infection.

Hanwei Li, Jinying Wang, Can Liu et al. · 0 citations
Aug 2026

Xanthomonas phaseoli pv. Manihotis effector XopAG impairs cassava immunity by hijacking MeHSP26 to suppress flavonoid biosynthesis.

Cassava bacterial blight (CBB), caused by Xanthomonas phaseoli pv. manihotis (Xpm), is a major disease constraining cassava production. Although overexpression of the Xpm effector XopAG enhances Arabidopsis susceptibility to Pseudomonas syringae pv. tomato DC3000, its virulence mechanism in cassava remains unclear. The study showed that deletion of XopAG did not affect morphology or extracellular enzyme production of Xpm, but significantly attenuated its virulence on cassava. Quantitative proteomic analysis revealed that 267 differentially accumulated proteins (DAPs) at 6 hours post-inoculation (hpi) and 429 DAPs at 6 days post-inoculation (dpi) were identified in cassava leaves inoculated with ΔxopAG mutant compared with Xpm. KEGG enrichment analysis showed that DAPs were significantly enriched in phenylpropanoid and flavonoid biosynthesis pathways. In the absence of XopAG, flavonoid biosynthesis-related proteins and genes (DFR, ANR, ANS, CYP75A1, FLS) were up-regulated, accompanied by increased total flavonoid content in cassava leaves during early infection. Furthermore, cassava small heat shock protein MeHSP26 was identified as a host target of XopAG, and two proteins interact in both cytoplasm and nucleus in N. benthamiana. Importantly, degradation assay reveals that XopAG promotes MeHSP26 degradation in N. benthamiana. Silencing MeHSP26 compromised cassava resistance to Xpm, following reducing flavonoid content and suppressing flavonoid gene expression. Together, these results demonstrate that XopAG promotes MeHSP26 degradation to suppress flavonoid biosynthesis, thereby attenuating cassava immunity during early Xpm inoculation. This work provides insights into cassava-Xpm interactions by revealing effector manipulation of metabolic pathways facilitates inoculation.

Liyun Yang, Yi-Xuan Wang, Dan Yang et al. · 0 citations

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