Histone deacetylases (HDACs) play essential roles in modulating chromatin structure to provide accessibility to gene regulators. Increasing evidence has linked HADCs to pathogenesis control in the filamentous plant fungi. However, its function remains unclear in Fusarium pseudograminearum, which has led to the emergence of the disease Fusarium crown rot in China. Here we identified the FpDEP1 gene, an orthologue of Saccharomyces cerevisiae DEP1 encoding a component of the Rpd3 histone deacetylase complex in F. pseudograminearum. The gene deletion mutant, ΔFpdep1, showed significantly retarded growth on PDA plates with reduced aerial hyphae formation. Pathogenicity tests displayed no typical leaf lesions and limited expansion capability of coleoptiles. Histopathological analysis indicated the ΔFpdep1 deletion mutant differentiated infectious hyphae and triggered massive reactive oxygen species (ROS) accumulation during the early infection stage, resulting in limited expansion to neighbor cells which was concurring with sensitivity to H₂O₂ and SDS tests in vitro. FM4-64 staining revealed that the ΔFpdep1 deletion mutant was delayed in endocytosis. The FpDEP1-GFP transgene complemented the mutant phenotypes and the fusion protein co-localized with DAPI staining, indicating that the FpDEP1 gene product is localized to the nucleus in spores and mycelia. Immunoprecipitation coupled with LC-MS/MS and yeast two-hybrid screening identified the Rpd3L-like HDAC complex containing at least FpDep1, FpSds3, FpSin3, FpRpd3, FpRxt3, FpCti6, FpRho23, and FpUme6. These results suggest that FpDep1 is involved in a HDAC complex functioning on fungal development and pathogenesis in F. pseudograminearum.

The hemibiotrophic pathogen Bipolaris sorokiniana causes root rot, leaf blotching, and black embryos in wheat and barley worldwide, resulting in significant yield and quality reductions. However, the mechanism underlying the host–pathogen interactions between B. sorokiniana and wheat or barley remains unknown. The B. sorokiniana genome encodes a large number of uncharacterized putative effector proteins. In this study, we identified a putative secreted protein, CsSp1, with a classic N‐terminal signal peptide, that is induced during early infection. A split‐marker approach was used to knock out CsSP1 in the Lankao 9‐3 strain. Compared with the wild type, the deletion mutant ∆Cssp1 displayed less radial growth on potato dextrose agar plates and produced fewer spores, and complementary transformation completely restored the phenotype of the deletion mutant to that of the wild type. The pathogenicity of the deletion mutant in wheat was attenuated even though appressoria still penetrated the host. Additionally, the infectious hyphae in the deletion mutant became swollen and exhibited reduced growth in plant cells. The signal peptide of CsSp1 was functionally verified through a yeast YTK12 secretion system. Transient expression of CsSp1 in Nicotiana benthamiana inhibited lesion formation caused by Phytophthora capsici. Moreover, CsSp1 localized in the nucleus and cytoplasm of plant cells. In B. sorokiniana‐infected wheat leaves, the salicylic acid‐regulated genes TaPAL, TaPR1, and TaPR2 were down‐regulated in the ∆Cssp1 strain compared with the wild‐type strain under the same conditions. Therefore, CsSp1 is a virulence effector and is involved in triggering host immunity.

Fusarium crown rot (FCR) in wheat is a prevalent soil-borne disease worldwide and poses a significant threat to the production of wheat (Triticum aestivum) in China, with F. pseudograminearum being the dominant pathogen. Currently, there is a shortage of biocontrol resources to control FCR induced by F. pseudograminearum, along with biocontrol mechanisms. In this study, we have identified 37 strains of biocontrol bacteria displaying antagonistic effects against F. pseudograminearum from over 8000 single colonies isolated from soil samples with a high incidence of FCR. Among them, QY43 exhibited remarkable efficacy in controlling FCR. Further analysis identified the isolate QY43 as Pseudomonas aeruginosa, based on its colony morphology and molecular biology. In vitro, QY43 significantly inhibited the growth, conidial germination, and the pathogenicity of F. pseudograminearum. In addition, QY43 exhibited a broad spectrum of antagonistic activities against several plant pathogens. The genomics analysis revealed that there are genes encoding potential biocontrol factors in the genome of QY43. The experimental results confirmed that QY43 secretes biocontrol factor siderophores and pyocyanin. In summary, QY43 exhibits a broad spectrum of antagonistic activities and the capacity to produce diverse biocontrol factors, thereby showing substantial potential for biocontrol applications to plant disease.

Fusarium pseudograminearum is one of the major fungal pathogens that cause Fusarium crown rot (FCR) worldwide and can lead to a substantially reduced grain yield and quality. Transcription factors play an important role in regulating growth and pathogenicity in plant pathogens. In this study, we identified a putative Zn(II)₂Cys₆ fungal-type domain-containing transcription factor and named it FpUme18. The expression of FpUME18 was induced during the infection of wheat by F. pseudograminearum. The ΔFpume18 deletion mutant showed defects in growth, conidial production, and conidial germination. In the responses to the cell wall, salt and oxidative stresses, the ΔFpume18 mutant inhibited the rate of mycelial growth at a higher rate compared with the wild type. The staining of conidia and mycelia with lipophilic dye FM4-64 revealed a delay in endocytosis when FpUME18 was deleted. FpUME18 also positively regulated the expression of phospholipid-related synthesis genes. The deletion of FpUME18 attenuated the pathogenicity of wheat coleoptiles. FpUME18 also participated in the production of the DON toxin by regulating the expression of TRI genes. Collectively, FpUme18 is required for vegetative growth, conidiation, stress response, endocytosis, and full virulence in F. pseudograminearum.