Analysis of the Difenoconazole-Resistance Risk and Its Molecular Basis in Colletotrichum truncatum from Soybean.

Autor: Shi N; Institute of Plant Protection, Fujian Academy of Agricultural Sciences, Fuzhou, Fujian 350013, China.; Fujian Key Laboratory for Monitoring and Integrated Management of Crop Pests, Fuzhou, Fujian 350013, China., Qiu D; Institute of Plant Protection, Fujian Academy of Agricultural Sciences, Fuzhou, Fujian 350013, China., Chen F; Institute of Plant Protection, Fujian Academy of Agricultural Sciences, Fuzhou, Fujian 350013, China.; Fujian Key Laboratory for Monitoring and Integrated Management of Crop Pests, Fuzhou, Fujian 350013, China., Yang YQ; Institute of Plant Protection, Jiangxi Academy of Agricultural Sciences, Nanchang, Jiangxi 330000, China., Du Y; Institute of Plant Protection, Fujian Academy of Agricultural Sciences, Fuzhou, Fujian 350013, China.; Fujian Key Laboratory for Monitoring and Integrated Management of Crop Pests, Fuzhou, Fujian 350013, China.
Jazyk: angličtina
Zdroj: Plant disease [Plant Dis] 2023 Oct; Vol. 107 (10), pp. 3123-3130. Date of Electronic Publication: 2023 Oct 16.
DOI: 10.1094/PDIS-12-22-2983-RE
Abstrakt: Anthracnose disease, caused by Colletotrichum truncatum , is a destructive fungal disease in soybean worldwide, and some demethylation inhibitor fungicides are used to manage it. In this study, the sensitivity of C. truncatum to difenoconazole was determined, and the risk for resistance development of C. truncatum to difenoconazole was also assessed. The results showed that the mean EC 50 value was 0.9313 μg/ml, and the frequency of sensitivity formed a unimodal distribution. Six stable mutants with a mutation frequency of 8.33 × 10 -5 were generated, and resistance factors ranged from 3.00 to 5.81 after 10 successive culture transfers. All mutants exhibited fitness penalties in reduced mycelial growth rate, sporulation, and pathogenicity, except for the Ct2-3-5 mutant. Positive cross-resistance was observed between difenoconazole and propiconazole but not between difenoconazole and prochloraz, pyraclostrobin, or fluazinam. One point mutation I463V in CYP51A was found in five resistant mutants. Surprisingly, the homologous I463V mutation has not been observed in other plant pathogens. CYP51A and CYP51B expression increased slightly in the resistant mutants as compared to wild-types when exposed to difenoconazole but not in the CtR61-2-3f and CtR61-2-4a mutants. In general, a new point mutation, I463V in CYP51A, could be associated with low resistance to difenoconazole in C. truncatum . In the greenhouse assay, control efficacy of difenoconazole on both parental isolates and the mutants increased in a dose-dependent manner. Collectively, the resistance risk of C. truncatum to difenoconazole is regarded to be low to moderate, suggesting that difenoconazole can still be reasonably used to control soybean anthracnose.
Competing Interests: The author(s) declare no conflict of interest.
Databáze: MEDLINE
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