Deletion of FgSRE1 Impairs Reproduction and Virulence of Fusarium graminearum and Alters Metabolic and Membrane-Transport Gene Expression

Identification of ZmGLN5, a candidate gene for resistance to Gibberella ear rot in maize

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.

The bZIP transcription factor PnAda1 functions as a regulator of virulence, fungicide tolerance and necrotrophy in the wheat pathogen Parastagonospora nodorum

It is shown that the understudied bZIP transcription factor PnAda1 is an important downstream component of this PnPf2-regulatory network, and current understanding of the transcriptional network underlying virulence, metabolism and stress adaptation in an important fungal wheat pathogen is expanded.

Monocarboxylate permease gene SsMP1 regulates Sporisorium scitamineum mating, pathogenicity and absorption and transport of citric acid

Sugarcane is an important sugar crop, and smut disease caused by Sporisorium scitamineum poses a severe threat with limited control measures. This study is based on transcriptome sequencing data from two distinct pathogenic strains of Sporisorium scitamineum generated in our laboratory. Among the significantly differentially expressed genes, we identified a gene predicted to encode a monocarboxylate permease, which we designated SsMP1. To investigate its biological function, SsMP1 knockout and complemented mutants were generated using PEG-mediated protoplast transformation. Our results showed that SsMP1 had little to no effect on sporidial morphology, colony morphology, growth rate, or tolerance to abiotic stresses. In the knockout mutant, SsMP1 expression was undetectable, whereas it was readily detected in both the wild-type and complemented strains, Moreover, the expression level in the complemented mutant was restored to that of the wild-type strain. Notably, sexual mating ability was almost completely abolished in the knockout mutant but was fully restored in the complemented mutant. Interestingly, supplementation with exogenous signaling molecules, including cAMP or tryptophol, largely rescued the mating defect of the knockout mutant. Consistently, the expression levels of Uac1, a gene involved in cAMP biosynthesis, and Aro8, a gene associated with tryptophol biosynthesis, were significantly lower in the knockout mutant than in the wild-type and complemented strains. In addition, the knockout mutant exhibited more than a 70% reduction in pathogenicity compared with the wild-type and complemented strains. Furthermore, citric acid transport and uptake were markedly impaired in the knockout mutant. Taken together, these findings suggest that SsMP1 may indirectly regulate the expression of key genes involved in the cAMP and tryptophol biosynthetic pathways, thereby modulating signaling molecule production and subsequently affecting mating and pathogenicity. In addition, SsMP1 appears to positively regulate citric acid uptake and transport in haploid sporidia. This study provides new molecular insights into the pathogenic mechanisms of S. scitamineum.

Systematic Identification of the GH28 Gene Family in the Pathogenic Fungus Cytospora pyri and Functional Verification of the Candidate Virulence Gene VP1G_08835

Findings demonstrate that GH28 genes participate in C. pyri infection and identify VP1G_08835 as an important GH28 member required for normal growth and contributing to virulence.

Autophagy-related protein 4 contributes to siderophore biosynthesis, toxin production, and virulence in Alternaria alternata.

It is demonstrated that AaAtg4 is important for spore germination, siderophore biosynthesis, iron acquisition, oxidative stress resistance, and toxin production, thereby establishing its critical role in A. alternata virulence.