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

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

Fusarium proliferatum is a postharvest pathogen responsible for severe rot in economically important fruits and vegetables, leading to food waste and safety concerns due to mycotoxin contamination. While the PHO signaling pathway is known to regulate phosphate homeostasis, its specific contribution to the virulence mechanisms of this foodborne pathogen remains unclear. In this study, we functionally characterized key components of the PHO pathway in F. proliferatum. Targeted deletion of PHO pathway genes (FpNuc1α, FpNuc1β, FpNuc2, FpPho80, and FpPho85) revealed their essential roles in vegetative growth, conidiation, and stress responses critical for surviving in storage environments. Transcription factor FpNuc1α is required for the full virulence of F. proliferatum. We demonstrate that FpNuc1α activity is tightly controlled by a phosphorylation switch in response to phosphate availability. Furthermore, we discovered that FpNuc1α recognizes a novel DNA motif (BSN) to directly activate FpGit1 gene, a glycerophosphodiester transporter required for full virulence. These findings uncover a specific regulatory mechnism linking phosphate sensing to the infection process of F. proliferatum, providing potential molecular targets for developing novel fungicides to control postharvest decay and ensure food safety.

Transcriptomic responses of Fusarium oxysporum f. sp. radicis-lycopersici to secreted antimicrobial compounds of Pseudomonas chlororaphis ToZa7

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

Fusarium sacchari is one of the major pathogenic fungi that cause sugarcane Pokkah Boeng disease (PBD). Effectors play pivotal roles in F. sacchari–sugarcane interaction; thus, characterizing these effectors is essential for elucidating the molecular mechanisms underlying F. sacchari pathogenicity and for developing effective strategies to control PBD. However, only a limited number of effectors have been functionally validated to date. Here, we report FsRGAE1, a candidate effector protein from F. sacchari predicted to encode a rhamnogalacturonan acetylesterase (RGAE). FsRGAE1 exhibits high expression during the early stages of infection and maintains relatively elevated expression levels throughout the F. sacchari–sugarcane interaction. Targeted deletion of the FsRGAE1 gene in F. sacchari had no discernible impact on mycelial growth, conidiation, or carbon-source utilization, yet it significantly attenuated fungal virulence. FsRGAE1 possesses both a signal peptide conferring secretory capacity and a transit peptide enabling its translocation into the host cytoplasm and nucleus. Using the Agrobacterium tumefaciens-mediated transient expression system in Nicotiana benthamiana, FsRGAE1 was confirmed to suppress cell death induced by Bcl-2-associated X protein (BAX), as well as ROS accumulation and callose deposition, and its nuclear localization is indispensable for this immunosuppressive activity. Collectively, these 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.

Transcriptome and Metabolome Dissection of Multilayered Pydiflumetofen Resistance Mechanisms in Fusarium graminearum

Wheat Fusarium head blight (FHB) is a globally prevalent and destructive fungal disease predominantly caused by Fusarium graminearum. Pydiflumetofen, a novel succinate dehydrogenase inhibitor (SDHI) fungicide, exhibits strong inhibitory activity against F. graminearum; however, the molecular regulatory mechanisms underlying the field-developed resistance in this pathogen remain poorly defined. In the present study, a field-evolved resistant isolate W24-039 and a sensitive isolate W24-016 were subjected to multi-omics analysis. The sequencing results identified compound mutations C89S/A93V in SdhC2, and A21T/S30F in SdhD of the resistant strain, which confer stable fungicide resistance without any detectable fitness costs. Physiological tests revealed that these target mutations sustain the homeostasis of succinate dehydrogenase (SDH) activity and intracellular ATP production. Following pydiflumetofen treatment, the sensitive isolate displayed remarkable declines in SDH activity, intracellular ATP content and deoxynivalenol (DON) biosynthesis, accompanied by markedly elevated cell membrane permeability. Transcriptomic sequencing uncovered 2221 differentially expressed genes (DEGs) in the sensitive strain under fungicide stress, and 2566 DEGs in the resistant isolate under the same conditions. The genes associated with detoxification and drug efflux, including cytochrome P450, glutathione S-transferase (GST), ABC and MFS transporters, were significantly upregulated in the resistant isolate. Metabolomic analysis indicated that differential metabolites were mainly enriched in the tricarboxylic acid (TCA) cycle, amino acid metabolism and membrane lipid biosynthesis pathways. The resistant strain maintained intact TCA cycle operation and accumulated high levels of pivotal metabolites such as phosphatidylcholine, unsaturated fatty acids and reduced glutathione. Integrated multi-omics analysis verified that the ABC transporter and glutathione metabolism pathways serve as core regulatory modules governing fungicide resistance. Collectively, F. graminearum develops resistance via the synergistic effects of SDH compound mutations, enhanced detoxification and efflux, and global metabolic remodeling, demonstrating that target-site mutation alone is not the sole driver of resistance, which is instead controlled by an intricate regulatory network involving multiple coordinated pathways. This study systematically characterizes the resistance regulatory network of F. graminearum against pydiflumetofen, and provides theoretical guidance for the rational application and sustainable field resistance management of this fungicide.

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.

The transcription factor CfMBZ1 of Colletotrichum fructicola governs host penetration to mediate Glomerella leaf spot pathogenesis in apple

Colletotrichum fructicola, the primary causal agent of Glomerella leaf spot (GLS), is a destructive fungal pathogen of apple, whose underlying pathogenic mechanisms remain largely unknown. A previous transcriptomic analysis of infected leaves indicated induction of the transcription factor CfMBZ1. This study confirmed that CfMBZ1 is highly expressed in conidia and during early infection. To elucidate its function, we generated a ΔCfMBZ1 deletion mutant via homologous recombination. Phenotypic analysis revealed that ΔCfMBZ1 lost pathogenicity on apple leaves due to a blockage in appressorium-mediated host penetration, despite retaining the ability to form penetration pegs on cellophane. However, extension of invasive hyphae and necrotrophic growth in wounded apple fruit were unaffected. The mutant also exhibited defects in maintaining the integrity of the cell wall and cell membrane, as well as in tolerating oxidative and acid–base stress. Comparative transcriptome analysis suggested that CfMBZ1 regulates appressorium-mediated penetration by modulating genes involved in peroxisome biogenesis, lipid droplet metabolism, and other penetration-related pathways. Our findings reveal that CfMBZ1 plays a critical role in the pathogenesis of Glomerella leaf spot caused by C. fructicola.