FpSmi1 regulates vegetative development, pathogenicity and fungicide sensitivity in Fusarium pseudograminearum

Fusarium pseudograminearum is the causal agent of Fusarium crown rot (FCR), which has caused severe yield losses in recent years. Currently, only a limited number of fungicides are registered for FCR control, highlighting the urgent need to develop novel fungicide targets. In addition to identifying essential and unique proteins as potential targets, recent research has increasingly focused on key proteins that serve as convergence points across multiple critical biological processes. Smi1 is a disordered hub protein that connects several essential cellular pathways, making it a promising candidate for fungicide development. However, the function of FpSmi1 in F. pseudograminearum remains unclear. In this study, deletion of FpSmi1 resulted in significant reductions growth rate and biomass. For asexual reproduction, the FpSmi1 deletion mutant exhibited decreased conidiation, shorter conidia, fewer septa per conidium, and shorter germ tube. Pathogenicity of the FpSmi1 deletion mutant was significantly attenuated on both wheat coleoptiles and wheat leaves. Furthermore, the FpSmi1 deletion mutant reduced its sensitivity to triazole fungicides by upregulating the expression levels of FpCyp51A and FpCyp51B . Additionally, the FpSmi1 deletion mutant showed changes in sensitivity to cell wall, cell membrane, and ionic stresses. Transcriptome analysis indicated that deletion of FpSmi1 affects the expression of genes involved in calcium-related pathways, thereby regulating the response to calcium ion stress. Collectively, FpSmi1 plays a critical role in F. pseudograminearum and represents a potential fungicide target for the control of FCR.