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The genus  Colletotrichum  contains a wide variety of important plant pathogens, and  Colletotrichum truncatum  is one of the most prevalent species of  Colletotrichum  on chili in China. Demethylation-inhibitor fungicides (DMIs) are currently registered chemical agents for the management of the anthracnose disease caused by  Colletotrichum  spp. To assess the risk for DMI resistance development, 112  C. truncatum  isolates were collected from infected pepper in 13 regions of China. The sensitivity of  C. truncatum  isolates to five DMI fungicides was determined based on mycelial growth inhibition assay.  C. truncatum  was sensitive to prochloraz, epoxiconazole, and difenoconazole, but not to tebuconazole or myclobutanil. Baseline sensitivity using the 112  C. truncatum  isolates was established for the first three effective DMIs. Prochloraz, epoxiconazole, and difenoconazole EC 50  values were 0.053 ± 0.023, 1.956 ± 0.815, and 1.027 ± 0.644 μg/ml, respectively. Eleven stable DMI-resistant mutants all exhibited lower fitness levels than their wild-type parents, suggesting a low risk of DMI resistance in  C. truncatum . By inducing gene expression,  CtCYP51  expression increased slightly in the resistant mutants as compared to wild-types when exposed to DMI fungicides and thus contributed at least partially to resistance. Molecular docking with CYP51 structure models was used to explain differential sensitivity of the DMI fungicides in  C. truncatum . Our results suggest that the M376L/H373N mutations in CYP51 changed the conformation of DMIs in the binding pocket. These changes prevented the formation of the Fe – N coordinate bond between the heme iron active site and tebuconazole or myclobutanil, and apparently contributed to tebuconazole and myclobutanil insensitivity of  C. truncatum .

Assessing the Risk for Resistance and Elucidating the Genetics of Colletotrichum truncatum That Is Only Sensitive to Some DMI Fungicides