Genome-Wide Association Study of Fungicide Sensitivity in a Fusarium graminearum Population Collected from North Dakota.

Abstract

Fusarium head blight is a destructive disease of small grains. The disease is predominantly caused by the haploid ascomycete fungus Fusarium graminearum in North America. To understand the genetics of quantitative traits for sensitivity to fungicides in this fungal pathogen, we conducted a genome-wide association study of sensitivity to two demethylation inhibition class fungicides, tebuconazole and prothioconazole, using an F. graminearum population of 183 isolates collected between 1981 and 2013 from North Dakota. Baseline sensitivity to tebuconazole and prothioconazole was established using 21 isolates collected between 1981 and 1994. Most fungal isolates were sensitive to both tebuconazole and prothioconazole; however, five isolates showed significantly reduced sensitivity to prothioconazole. The genome-wide association study identified one significant marker-trait association on chromosome 3 for tebuconazole resistance, whereas six significant marker-trait associations, one on chromosome 1, three on chromosome 2, and two on chromosome 4, were detected for prothioconazole resistance. Functional annotation of the marker-trait association for tebuconazole revealed a candidate gene encoding a basic helix-loop-helix domain-containing protein that reinforces sterol in the fungal membrane. Putative genes for prothioconazole resistance were also identified, which are involved in RNA interference, the detoxification by ubiquitin-proteasome pathway, and membrane integrity reinforcement. Considering the potential of the pathogen toward overcoming chemical control, continued monitoring of fungal sensitivities to commercially applied fungicides, especially those containing prothioconazole, is warranted to reduce risks of fungicide resistance in the pathogen populations.