The P2A-ATPase FgPMR1 regulates growth, pathogenicity, and phenamacril sensitivity of Fusarium graminearum by...

Fusarium graminearum, the causal agent of Fusarium head blight (FHB), poses a severe threat to wheat production by reducing yield and contaminating grains with mycotoxins like deoxynivalenol (DON). PMR1, a member of the P-ATPase family, is known for its conserved roles in ion homeostasis and secretory pathways in yeast. However its functions in F. graminearum remain unclear. This study systematically investigated the regulatory roles of FgPMR1 in F. graminearum. The findings indicate that FgPMR1 partial co-localization with Golgi apparatus (GA). Deletion of FgPMR1 significantly impairs vegetative growth, asexual reproduction, pathogenicity, and DON synthesis in F. graminearum. Its knockout results in an approximate 30% decrease in the mycelial growth rate, about an 85% reduction in spore production, and a roughly 50% decrease in DON synthesis. Importantly, deletion of FgPMR1 significantly increases the sensitivity of F. graminearum to phenamacril. This regulatory mechanism involves FgPMR1 interacting with FgMyo-5 and FgAct to modulate phenamacril sensitivity. The phenamacril-induced upregulation of FgMyo-5 and FgAct expression in the ΔFgPMR1 mutant was significantly attenuated relative to that in the PH-1 strain. Overall, this study elucidates the multifunctional regulatory role of FgPMR1 in F. graminearum. These findings provide novel insights into the molecular mechanisms governing fungal virulence and fungicide sensitivity.