FolIws1-driven nuclear translocation of deacetylated FolTFIIS ensures conidiation of Fusarium oxysporum.

Plant diseases caused by fungal pathogens pose a great threat to crop production. Conidiation of fungi is critical for disease epidemics and serves as a promising drug target. Here, we show that deacetylation of the FolTFIIS transcription elongation factor is indispensable for Fusarium oxysporum f. sp. lycopersici (Fol) conidiation. Upon microconidiation, Fol decreases K76 acetylation of FolTFIIS by altering the level of controlling enzymes, allowing for its nuclear translocation by FolIws1. Increased nuclear FolTFIIS enhances the transcription of sporulation-related genes and, consequently, enables microconidia production. Deacetylation of FolTFIIS is also critical for the production of macroconidia and chlamydospores, and its homolog has similar functions in Botrytis cinerea. We identify two FolIws1-targeting chemicals that block the conidiation of Fol and have effective activity against a wide range of pathogenic fungi without harm to the hosts. These findings reveal a conserved mechanism of conidiation regulation and provide candidate agrochemicals for disease management.

Paralogous Cyp51s mediate the differential sensitivity of Fusarium oxysporum to sterol demethylation inhibitors.

BACKGROUND: As a soilborne fungus, Fusarium oxysporum can cause vascular wilt in numerous economically important crops. Application of antifungal drugs is the primary method for the control of F. oxysporum. Cyp51, a key enzyme of sterol biosynthesis is the main target of sterol demethylation inhibitors. RESULTS: The F. oxysporum genome contains three paralogous CYP51 genes (named FoCYP51A, FoCYP51B and FoCYP51C) that putatively encode sterol 14α-demethylase enzymes. Each of the three genes was able to partially complement the Saccharomyces cerevisiae ERG11 mutant. Growth assays demonstrated that deletion mutants of FoCYP51B, but not FoCYP51A and FoCYP51C were significantly retarded in hyphal growth. Deletion of FoCYP51A (ΔFoCyp51A and ΔFoCyp51AC) led to increased sensitivity to 11 sterol demethylation inhibitors (DMIs). Interestingly, FoCYP51B deletion mutants (ΔFoCyp51B and ΔFoCyp51BC) exhibited significantly increased sensitivity to only four DMIs (two of which are in common with the 11 DMIs mentioned earlier). Deletion of FoCYP51C did not change DMI sensitivity of F. oxysporum. None of the three FoCYP51s are involved in F. oxysporum virulence. The sensitivity of F. oxysporum isolates increased significantly when subjected to a mixture of different subgroups of DMIs classified based on the different sensitivities of FoCYP51 mutants to DMIs compared to the individual components. CONCLUSIONS: FoCYP51A and FoCYP51B are responsible for sensitivity to different azoles. These findings have direct implications for fungicide application strategies of plant and human diseases caused by F. oxysporum. © 2018 Society of Chemical Industry.