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唑醚菌酯分离株的生存成本及其不同的分子机制。

Survival Cost and Diverse Molecular Mechanisms of Isolate Resistance to Epoxiconazole.

机构信息

Key Laboratory of Pesticide and Chemical Biology of the Ministry of Education, College of Chemistry, Central China Normal University, Wuhan, China.

College of Plant Protection, Northwest Agriculture and Forestry University, Yangling, China.

出版信息

Plant Dis. 2021 Feb;105(2):473-480. doi: 10.1094/PDIS-02-20-0393-RE. Epub 2020 Dec 21.

DOI:10.1094/PDIS-02-20-0393-RE
PMID:33349002
Abstract

Rice blast caused by is one of the most destructive diseases on rice worldwide. Epoxiconazole is a 14α-demethylation inhibitor (DMI) with excellent control on rice blast; to date, no resistant isolates have been observed in the field. Four mutants resistant to epoxiconazole were generated from three parental isolates via fungicide adaptation. Resistance was stable after 10 weekly consecutive transfers on fungicide-free medium. Three parameters, including growth rate, sporulation in vitro, and aggressiveness, were significantly lower for mutants compared with their parental isolates, with the exception of the low-resistance isolate. Sporulation and aggressiveness were negatively correlated with effective concentration values for 50% inhibition of mycelial growth for parental isolates and mutants ( < 0.05). Cross-resistance was found between epoxiconazole and prochloraz (ρ = 0.863, = 0.000) or difenoconazole (ρ = 0.861, = 0.000). The resistance factor for mutants was positively correlated with the relative expression of in epoxiconazole treatment ( = 0.977, = 0.02). In addition, two putative amino acid substitutions in MoCYP51A were found in two resistant mutants: Y126F in the high-resistance mutant and I125L in the low-resistance mutant. Mutation Y126F reduced the affinity of MoCYP51A with epoxiconazole, whereas I125L was not in the binding pocket of epoxiconazole. No amino acid change or overexpression in MoCYP51B was found in any of the mutants studied. To our knowledge, this is the first study to report DMI resistance observed in . The survival cost of resistance to epoxiconazole might be the reason why DMI resistance has not yet emerged in field populations worldwide.

摘要

稻瘟病由 引起,是全球范围内对水稻危害最大的疾病之一。环丙唑醇是一种具有优异防治稻瘟病效果的 14α-去甲基化抑制剂(DMI);迄今为止,田间尚未观察到对其有抗性的分离株。本研究通过杀菌剂驯化,从 3 个原始分离株中获得了对环丙唑醇具有抗性的 4 个突变体。在无杀菌剂的培养基上连续 10 周传代后,抗性仍然稳定。与亲本分离株相比,除低抗性分离株外,突变体的生长速率、体外产孢和侵袭力这 3 个参数均显著降低,突变体亲本分离株的有效浓度值(EC50)对菌丝生长的抑制率与产孢量和侵染力呈负相关(<0.05)。突变体与环丙唑醇和丙环唑(ρ=0.863,=0.000)或氟环唑(ρ=0.861,=0.000)之间存在交叉抗性。突变体的抗性因子与环丙唑醇处理中 MoCYP51A 的相对表达呈正相关(=0.977,=0.02)。此外,在 2 个高抗性和 1 个低抗性突变体中发现了 MoCYP51A 中的 2 个假定氨基酸替换:高抗性突变体中的 Y126F 和低抗性突变体中的 I125L。突变体 Y126F 降低了 MoCYP51A 与环丙唑醇的亲和力,而 I125L 不在环丙唑醇的结合口袋中。在研究的所有突变体中均未发现 MoCYP51B 的氨基酸变化或过表达。据我们所知,这是首次报道在 中观察到 DMI 抗性。对环丙唑醇的 DMI 抗性的生存代价可能是其在全球田间种群中尚未出现的原因。

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