The fungal effector CvA10999 suppresses plant immunity by targeting VvSnRKb1 to facilitate Colletotrichum viniferum virulence.

Down-regulation of VvPLL3 enhances grapevine resistance to Erysiphe necator via defense activation and cell wall remodeling.

An apoplastic effector Uv7366 contributes to Ustilaginoidea virens virulence and elicits plant immunity.

Ustilaginoidea virens (Cook) Takahashi, the causal agent of rice false smut disease (RFS), causes severe losses in yield and grain quality worldwide. The ascomycete pathogen deploys a large arsenal of effectors to facilitate infection, but only a few have been functionally characterized. In this study, we characterized Uv7366, an apoplastic glycoside hydrolase family 12 (GH12) protein that was previously identified in the culture filtrate of U. virens. Purified Uv7366 triggered a reactive oxygen species (ROS) burst and strongly induced the transcription of multiple defense-associated genes, and pretreatment of rice (Oryza sativa L.) and Nicotiana benthamiana plants with Uv7366 enhanced their disease resistance. Uv7366 was strongly induced during host invasion and targeted deletion of this gene in U. virens substantially attenuated virulence on rice. Collectively, our findings demonstrate that Uv7366 facilitates U. virens infection while also being recognized by the plant innate immune system, providing new insights into the pathogenic mechanisms of U. virens and potential strategies for the biocontrol of RFS.

A VvWRKY8-salicylic acid pathway amplification loop confers resistance to Plasmopara viticola in grapevine

To defend against pathogen invasion, plants deploy a variety of strategies, among which salicylic acid (SA), a key plant defense hormone, plays crucial roles in enhancing host resistance to biotrophic and semibiotrophic microbes. Although numerous studies elucidated mechanisms of the SA signaling pathway, many questions remain. In this study, we show that the group IIc WRKY transcription factor VvWRKY8 is involved in grape (Vitis vinifera) defense responses to the oomycete pathogen Plasmopara viticola, as indicated by transcriptome analyses. VvWRKY8 increases the expression of defense-related genes and SA accumulation, thereby promoting grape resistance to P. viticola. Further analyses reveal that VvWRKY8 is recruited to the promoters of VvCBP60g and VvSARD1, which encode two key regulators of SA biosynthesis, and upregulates their transcription. Moreover, VvWRKY8 transcription is induced by SA and by two bZIP transcription factors, VvTGA2a and VvTGA2b, which cooperate with the SA receptors VvNPR1 and VvNPR3 to modulate the expression of SA-responsive genes. Collectively, our results indicate that a positive feedback loop involving VvWRKY8 and the SA pathway components VvCBP60g, VvSARD1, and VvTGA2a/2b functions in response to P. viticola attack in grapevine.

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.

Effector FsSCR6 contributes to the virulence of Fusarium sacchari on sugarcane and suppresses plant immunity.

Pokkah Boeng disease caused by Fusarium sacchari seriously threatens the yield and quality of sugarcane worldwide. Effectors play a crucial role in the infection and colonization of pathogens. However, there were few reports on the virulence functions of F. sacchari effectors. To characterize effector functions and unravel the pathogenic mechanisms of F. sacchari, we identified an effector FsSCR6, which was vital for the virulence of F. sacchari. Gene knockout mutants showed no difference in growth rates and colony morphology from wild-type. However, the virulence of knockout mutants was severely impaired. Agrobacterium-mediated transient expression assays in Nicotiana benthamiana showed that FsSCR6 and FsSCR6Δsp (without signal peptide) performed cell death-suppressive activity inside plant cells. 3'3-diaminobenzidine staining and aniline blue staining assays showed that FsSCR6 significantly reduced the accumulation of reactive oxygen species and callose deposition triggered by BCL-2-Associated X protein (BAX) in N. benthamiana leaves. FsSCR6 significantly suppressed the relative expression of the marker genes of the hypersensitive responses and salicylic acid (SA)-, jasmonic acid (JA)-, and ethylene-dependent immunity in N. benthamiana. Overall, FsSCR6 is required for F. sacchari virulence; it performs a function inside plant cells and suppresses the plant immune responses by regulating the SA-, JA- and ethylene-mediated defense pathways. These results clarify the function of this effector from F. sacchari and assist in dissecting the interaction between sugarcane and F. sacchari, ultimately contributing to sugarcane production.

The role of Fusarium oxysporum effector protein Avr2 in resistance and pathogenicity

It is shown that expression of AVR2 is strongly induced in root-and xylem-colonizing hyphae three days post inoculation, and it is found that Avr2 has to be nuclear localized to trigger an I-2 -dependent cell death response.