FpNuc1α regulates phosphate signaling and pathogenicity in Fusarium proliferatum infection of jujube fruit by targeting FpGit1 via a novel BSN motif.

FpLaeA Coordinates Fusarium proliferatum Pathogenesis by Orchestrating Mycotoxin Biosynthesis and Host Immune Subversion

It is reported that the methyltransferase FpLaeA is a global regulator essential for F. proliferatum pathogenicity and a target for integrated control of F. proliferatum and its associated mycotoxin risk.

MdLYK7 enhances resistance to Valsa canker by activating salicylic acid signaling and PbeBGLU12-mediated fungal cell wall stress.

A Rhamnogalacturonan Acetylesterase Effector FsRGAE1 Enhances the Virulence of Fusarium sacchari by Localizing to the Nucleus and Suppressing Plant Immunity

Findings indicate that FsRGAE1 promotes F. sacchari virulence by suppressing host immune responses in a nuclear localization-dependent manner, providing new insights into effector-mediated F. sacchari pathogenesis and potential target for resistance breeding in sugarcane.

TrcrtB regulates carotenoid biosynthesis, stress tolerance, conidiation and pathogenicity in the postharvest pink rot fungus, Trichothecium roseum.

The results suggest that TrcrtB and phytoene are critical for development, stress tolerance and pathogenicity of T. roseum and highlight the roles of TrcrtB and phytoene in the pathogenic fungus T. roseum.

PpTOR, a Major Factor Associated with Phytophthora parasitica Virulence, Serves as a Candidate RNAi Target for Disease Control

Phytophthora parasitica is a devastating oomycete pathogen that causes significant crop losses worldwide. Identifying master regulators of its virulence is crucial for the development of novel control strategies. Here, we demonstrate that the conserved eukaryotic kinase TOR (target of rapamycin) is essential for both growth and pathogenicity in P. parasitica. Transcriptomic analysis revealed that PpTOR inhibition broadly reprograms the transcriptome of P. parasitica, notably leading to the downregulation of numerous PpRxLR and PpCRN effector genes. Among these genes, the overexpression of PpRxLR3 increased plant susceptibility to P. parasitica by affecting jasmonic acid biosynthesis and signaling. On the basis of the crucial role of PpTOR, we evaluated its potential as a target for intervention. Host-induced gene silencing (HIGS) of PpTOR in Nicotiana benthamiana conferred strong resistance to P. parasitica, which was associated with the downregulation of the expression of PpTOR and key effector genes during P. parasitica infection. Furthermore, small RNA sequencing confirmed the production of PpTOR-specific siRNAs in HIGS plants. Exogenous application of synthetic siRNAs targeting PpTOR effectively reduced P. parasitica virulence. Our findings establish PpTOR as a global regulator of pathogenicity and validate PpTOR as a promising target for RNA-based disease control strategies.

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.