T-DNA Mutagenesis Reveals FpPer1 as a Dual-Function Regulator of Virulence and Fungicide Resistance in Fusarium pseudograminearum.

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.