Exserohilum rostratum is a causal agent of severe maize leaf spot, posing a threat to maize production. Carbohydrate esterase (CE) can catalyze the removal of acyl modifications from plant cell wall polysaccharides, thereby promoting polysaccharide hydrolysis. A total of 87 CE genes were identified in the E. rostratum ER1 genome. In this study, we conducted a comprehensive analysis of the E. rostratum CE (ErCE) genes, including physicochemical properties, structural features, promoter cis-acting regulatory elements, and functional analysis. Subcellular localization analysis revealed that more than half of ErCEs were located extracellular. ErCEs contain abundant conserved domains, indicating functional diversity of these proteins. The promoter region of ErCE genes contains a rich variety of cis-acting regulatory elements related to plant hormone regulation, stress response, and developmental processes. Functional enrichment analysis indicated that ErCE genes are predominantly involved in metabolic pathways. In addition, the expression pattern revealed significant changes in ErCE genes during E. rostratum infection, indicating that they play an important role in pathogen invasion and lesion expansion. Overall, this study elucidated the structural characteristics and expression patterns of the CE genes in E. rostratum, providing conditions for further exploration of their roles in fungal pathogenesis and laying the foundation for the improvement of sustainable agricultural systems using related genes.

Fusarium crown rot (FCR), caused by Fusarium pseudograminearum, is a devastating wheat disease leading to significant yield losses worldwide. However, the pathogenic mechanism of F. pseudograminearum and its resistance to fungicides remain poorly understood. In this study, we identified a hypothetical gene encoding GPI-anchored protein, designated FpPer1, by screening a T-DNA insertion mutant library of F. pseudograminearum for tebuconazole resistance. The ΔFpper1 mutant exhibited increased sensitivity to the triazole antifungal drugs and fludioxonil. Additionally, the deletion of FpPER1 impaired fungal growth, conidiation, and pathogenicity in barley leaves and wheat coleoptiles. Furthermore, the ΔFpper1 mutant displayed enhanced susceptibility to various environmental stresses, including NaCl, CR, sorbitol, H₂O₂, and SDS. The mutant also showed reduced penetration peg formation and impaired reactive oxygen species (ROS) scavenging ability during infection. Subcellular localization analysis revealed that FpPer1-GFP co-localized with the endoplasmic reticulum (ER) marker RFP-HDEL in both conidia and hyphae, indicating its localization in the ER. In summary, our findings demonstrate that FpPER1 plays an important role in pathogenicity and fungicide resistance in F. pseudograminearum. This study not only provides a theoretical foundation for understanding fungal virulence mechanisms but also offers practical insights for developing novel fungicide strategies.