Genome-wide association study of DMI fungicide sensitivity detects numerous small-effect variants in the major North American population of Fusarium graminearum

Fusarium head blight (FHB), a major disease of wheat, is primarily managed through applications of demethylation inhibitor (DMI) fungicides during anthesis. However, repeated use of DMIs has led to the emergence of Fusarium graminearum isolates with reduced sensitivity and, in some cases, resistance. In this study, we evaluated the sensitivity of 152 F. graminearum isolates to propiconazole and tebuconazole. While sensitivity varied among isolates, no resistant strains were detected. We also conducted a genome-wide association study (GWAS) to investigate the genetic basis of DMI sensitivity. GWAS identified 48 and 39 quantitative trait nucleotides (QTNs) associated with propiconazole and tebuconazole sensitivity, respectively, with 12 QTNs common to both fungicides—supporting their common mode of action. Candidate gene analysis highlighted genes encoding transporters, secondary metabolite synthesis enzymes, transcription factors, and a heat shock protein as potential candidates for DMI fungicide response. We propose that tolerance to DMIs in F. graminearum is linked to active fungicide efflux out of fungal cells, mediated by transporters, including those associated with secondary metabolite pathways.