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

Frontiers in Microbiology

卷:8

Hongxia Duan¹  Can Zhang²  Weizhen Wang²  Muhammad Imran²  Xili Liu²  Jianjun Hao³  Yongzhao Diao⁴ 

[1] Department of Applied Chemistry, China Agricultural UniversityBeijing, China;

[2] Department of Plant Pathology, China Agricultural UniversityBeijing, China;

[3] School of Food and Agriculture, University of Maine, OronoME, United States;

[4] State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of SciencesBeijing, China;

关键词: Colletotrichum truncatum;    DMI fungicides;    mechanism of sensitivity differentiation;    M376L/H373N;    resistance analysis;   

DOI  :  10.3389/fmicb.2017.01779

来源: DOAJ

【 摘 要 】

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 EC50 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.

【 授权许可】

Unknown