The paper in Nature Communications is here: https://www.nature.com/articles/s41467-019-09145-6
Fusarium graminearum, a member of the F. graminearum species complex, is the most prevalent and aggressive pathogen of Fusarium head blight (FHB) in cereal crops worldwide, especially in wheat. Severe FHB epidemics have occurred in China and many other wheat-growing regions of the world since 2010. In addition to enormous yield losses, FHB pathogens have serious potential impact on human and animal health by contaminating wheat, barley, and maize with various mycotoxins. The increase of FHB incidence may be attributable to global warming, reduced tillage, and the practice of heavily returning straws to the field. On the basis of the economic importance of FHB and trichothecene toxicity, F. graminearum has be as listed as one of the top 10 fungal plant pathogens.
Currently, application of chemical fungicides is still important approach to control FHB in many regions of the world because of the lack of effective disease-resistant wheat cultivars. Demethylation inhibitor (DMI) class fungicides, especially tebuconazole, and prothioconazole, block fungal sterol biosynthesis and are the most widely used and relatively effective fungicides for the control of FHB and reduction of mycotoxin accumulation.
In the last ten years, we have collected more than 100,000 strains of F. graminearum in the wheat fields treated with multi-applications of DMIs, but did not find any highly DMI-resistant strains. However, we did find F. graminearum is able to develop genetically instable tolerance to DMI easily, although these DMI-tolerant strains will recover their fungicide sensitivity after growth on PDA medium without DMI treatment. In practices, two applications of DMIs per season are often required in the year of FHB epidemic. The first application of DMI may induce fungicide tolerance in F. graminearum, which leads to a decline in fungicide efficacy of the second application.
The tolerance of F. graminearum to DMI results from the overexpression of fungicide target genes (FgCYP51s) induced by DMI treatment. In this study, we found that the transcription factor FgSR plays an important role in regulating FgCYP51 expression. In addition, we found that the FgSR mutant is unable to develop tolerance to DMIs, indicating this transcription factor is a potential target for the management of DMI tolerance in F. graminearum and likely in other fungi of Sordariomycetes and Leotiomycetes.