Investigating Selection of Demethylation Inhibitor Fungicide Insensitive Sclerotinia Homoeocarpa Isolates By Boscalid, Flurprimidol, and Paclobutrazol

Dollar spot, caused by Sclerotinia homoeocarpa F.T. Bennett, is the most economically important disease of golf course turfgrass in the northern United States. Fungicide resistance, especially to demethylation inhibitor (DMI) fungicides, is common for S. homoeocarpa. Plant growth regulators (PGRs) are commonly applied on golf courses and have a similar chemistry to DMIs. Previous research has suggested multiple resistance among the PGRs flurprimidol and paclobutrazol, the succinase dehydrogenase inhibitor fungicide boscalid, and the DMI propiconazole, with evidence for the involvement of the multidrug efflux transporter gene, ShPDR1. The objective of this research was to investigate if flurprimidol, paclobutrazol, and boscalid select for DMI insensitivity in the field. We tested eight treatments: flurprimidol alone, tank-mixed with propiconazole, and rotated with propiconazole; paclobutrazol alone, tank-mixed with propiconazole, and rotated with propiconazole; propiconazole alone; and boscalid alone. S. homoeocarpa was isolated from infected turfgrass three times per year in 2010 and 2011 following treatment applications. A significant shift in DMI insensitivity was observed from the initial sampling in 2010 to the final sampling in 2011 for all treatments, except the PGRs alone and the untreated control. Both PGRs induced overexpression of ShPDR1, and we confirmed the functional involvement of ShPDR1 in reducing S. homoeocarpa sensitivity to PGRs using the ShPDR1 overexpressing yeast mutant. These results have important implications for managing DMI resistance, further investigating the fungistatic activity of PGRs, and developing new fungicides for S. homoeocarpa.