FgNR gene regulates growth, pathogenicity, and fungicide sensitivity in Fusarium graminearum

Fusarium graminearum is the predominant pathogenic fungus causing Fusarium head blight, posing significant threats to food security and agricultural development. In this study, gene knockout technology was employed to construct FgNR (nitrate reductase gene) knockout and complemented mutants of F. graminearum to investigate the biological functions of FgNR. The results demonstrated that deletion of FgNR significantly reduced the growth rate and conidial germination rate of F. graminearum. The knockout mutants were unable to grow on basic medium containing only nitrate, while the wild type and complementation grew normally. The growth rate of ΔFgNR was enhanced under NaCl and KCl stress. Furthermore, ΔFgNR exhibited compromised cell membrane and cell wall integrity, as well as reduced tolerance to external oxidants. Additionally, the pathogenicity of ΔFgNR was significantly attenuated, accompanied by decreased deoxynivalenol (DON) production. The expression levels of Tri5 and Tri6 genes were downregulated, whereas the expression level of Tri10 was upregulated in the mutant strain. Compared to the wild-type strain, the knockout mutant exhibited decreased sensitivity to prothioconazole, accompanied by a marked increase in FgCYP51A gene expression. These findings indicate that FgNR plays critical roles in asexual reproduction, pathogenicity, nitrogen source utilization, and responses to abiotic stress and fungicide sensitivity in F. graminearum.