Researchers have identified a single fungal protein, FpSmi1, as a key controller of multiple biological processes in Fusarium pseudograminearum, the causal agent of Fusarium crown rot, a disease that has caused severe yield losses in wheat in recent years. The findings, published as an open access research article in BMC Plant Biology, suggest that FpSmi1 could serve as a potential target for the development of new fungicides.
Fusarium crown rot currently has only a limited number of registered fungicides available for its control, a gap that the authors describe as creating an urgent need for novel fungicide targets. Rather than focusing solely on essential or unique fungal proteins, recent research has increasingly examined proteins that act as convergence points across several critical cellular pathways, since disrupting such hubs could interfere with multiple fungal functions at once.
Smi1 belongs to this category: it is a disordered hub protein that connects several essential cellular pathways. Until this study, the function of its counterpart in F. pseudograminearum, FpSmi1, remained unclear. The research team addressed this gap by deleting the FpSmi1 gene and examining the consequences for the fungus’s growth, reproduction, virulence and stress responses.
The deletion had a marked effect on vegetative development. Mutant strains lacking FpSmi1 showed significant reductions in both growth rate and biomass compared with the intact fungus, indicating that the protein supports basic vegetative fitness.
Asexual reproduction was also impaired. The FpSmi1 deletion mutant produced fewer conidia, the fungal spores responsible for spread, and the conidia that were produced were shorter, contained fewer septa per conidium, and generated shorter germ tubes. These changes suggest that FpSmi1 influences both how many spores the fungus makes and how those spores are built.
Pathogenicity tests showed that the mutant’s ability to cause disease was significantly attenuated on both wheat coleoptiles and wheat leaves. The reduced virulence, combined with the growth and sporulation defects, reinforces the picture of FpSmi1 as a protein with wide-reaching roles in the fungus’s lifecycle.
Perhaps most striking for fungicide development, the deletion mutant showed reduced sensitivity to triazole fungicides. The mutant also displayed altered sensitivity to stresses affecting the cell wall, the cell membrane and ionic balance.
Transcriptome analysis provided a mechanistic clue: deletion of FpSmi1 affected the expression of genes involved in calcium-related pathways, and the mutant’s response to calcium ion stress was altered accordingly. This connects FpSmi1 to calcium signalling as one of the cellular pathways it helps regulate.
Taken together, the results position FpSmi1 as a critical node in F. pseudograminearum, linking vegetative growth, spore formation, disease-causing ability, stress tolerance and fungicide sensitivity. The authors conclude that the protein represents a potential fungicide target for the control of Fusarium crown rot, a crop disease for which treatment options remain limited.
Subject of Research: The role of the FpSmi1 protein in the growth, pathogenicity and fungicide sensitivity of the wheat crown rot fungus Fusarium pseudograminearum
Article Title: FpSmi1 regulates vegetative development, pathogenicity and fungicide sensitivity in Fusarium pseudograminearum
Article References: Li, L., Li, J., Li, X., Li, S., Wang, H., Liu, R., & Wu, L. (2026). FpSmi1 regulates vegetative development, pathogenicity and fungicide sensitivity in Fusarium pseudograminearum. BMC Plant Biology. https://doi.org/10.1186/s12870-026-10289-z
Image Credits: AI Generated
DOI: 10.1186/s12870-026-10289-z
Keywords: Fusarium pseudograminearum, Fusarium crown rot, FpSmi1, fungicide target, triazole fungicides, wheat, fungal pathogenicity, conidiation, Cyp51, calcium signalling, gene deletion, transcriptomics
News Source: Alan Morgan. (October 29, 2026). Fungal protein FpSmi1 shapes growth, virulence and fungicide response in wheat pathogen. Scienmag.



