Resistant risk and resistance mechanism of florylpicoxamid in Colletotrichum gloeosporioides isolated from Chinese walnut

IF 4.2 1区农林科学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pesticide Biochemistry and Physiology Pub Date : 2024-08-18 DOI:10.1016/j.pestbp.2024.106093

{"title":"Resistant risk and resistance mechanism of florylpicoxamid in Colletotrichum gloeosporioides isolated from Chinese walnut","authors":"","doi":"10.1016/j.pestbp.2024.106093","DOIUrl":null,"url":null,"abstract":"<div>Colletotrichum gloeosporioides is the causal pathogen for the devastating walnuts anthracnose. A novel quinone inside inhibitor (QiI) fungicide florylpicoxamid has strong inhibitory efficacy against C. gloeosporioides. This study looked into the resistance risk and mechanism of C. gloeosporioides to florylpicoxamid. The basal level sensitivity of C. gloeosporioides isolates (n = 102) to florylpicoxamid was established with an average 50% mycelial growth inhibition concentration (EC50) value of 0.069 ± 0.035 μg/mL. Six stable florylpicoxamid-resistant mutants with resistance factors of >1000 were produced. The fitness of every mutant was much lower than that of their parental isolates. In general, the resistance risk of C. gloeosporioides to florylpicoxamid would be moderate. Molecular docking results revealed that the amino acid substitutions A37V, and S207L in CgCytb lead to a reduction in the binding affinity between florylpicoxamid and CgCytb, indicating that these two mutations (S207L and A37V in CgCytb) indeed confer florylpicoxamid resistance in C. gloeosporioides. These findings offer a fresh viewpoint on the mechanism underlying QiI fungicide resistance and could support the prudent application of florylpicoxamid in the future to combat walnut anthracnose.</div>","PeriodicalId":19828,"journal":{"name":"Pesticide Biochemistry and Physiology","volume":null,"pages":null},"PeriodicalIF":4.2000,"publicationDate":"2024-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pesticide Biochemistry and Physiology","FirstCategoryId":"97","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0048357524003262","RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Colletotrichum gloeosporioides is the causal pathogen for the devastating walnuts anthracnose. A novel quinone inside inhibitor (QiI) fungicide florylpicoxamid has strong inhibitory efficacy against C. gloeosporioides. This study looked into the resistance risk and mechanism of C. gloeosporioides to florylpicoxamid. The basal level sensitivity of C. gloeosporioides isolates (n = 102) to florylpicoxamid was established with an average 50% mycelial growth inhibition concentration (EC₅₀) value of 0.069 ± 0.035 μg/mL. Six stable florylpicoxamid-resistant mutants with resistance factors of >1000 were produced. The fitness of every mutant was much lower than that of their parental isolates. In general, the resistance risk of C. gloeosporioides to florylpicoxamid would be moderate. Molecular docking results revealed that the amino acid substitutions A37V, and S207L in CgCytb lead to a reduction in the binding affinity between florylpicoxamid and CgCytb, indicating that these two mutations (S207L and A37V in CgCytb) indeed confer florylpicoxamid resistance in C. gloeosporioides. These findings offer a fresh viewpoint on the mechanism underlying QiI fungicide resistance and could support the prudent application of florylpicoxamid in the future to combat walnut anthracnose.

Abstract Image

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

从中国核桃中分离的球孢子菌对氟啶虫酰胺的抗性风险和抗性机理

球孢子菌（Colletotrichum gloeosporioides）是毁灭性核桃炭疽病的病原菌。一种新型醌内抑制剂（QiI）杀菌剂氟啶虫酰胺（florylpicoxamid）对球孢子菌有很强的抑制作用。本研究探讨了球孢子菌对氟啶虫酰胺的抗性风险和机制。研究确定了球孢子菌分离株（n = 102）对氟啶虫酰胺的基本敏感性，其平均50%菌丝生长抑制浓度（EC50）值为0.069 ± 0.035 μg/mL。产生了 6 个稳定的抗氟啶虫酰胺突变体，其抗性因子为 1000。每个突变体的适应性都远远低于其亲本分离物。一般来说，球孢子菌对氟啶虫酰胺的抗性风险为中等。分子对接结果显示，CgCytb中的氨基酸取代A37V和S207L导致氟啶虫酰胺与CgCytb之间的结合亲和力降低，表明这两个突变（CgCytb中的S207L和A37V）确实使球孢子菌对氟啶虫酰胺产生抗性。这些发现为研究 QiI 杀菌剂的抗性机理提供了新的视角，有助于今后谨慎使用氟啶虫酰胺防治核桃炭疽病。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

Pesticide Biochemistry and Physiology 生物-昆虫学

CiteScore

7.00

自引率

8.50%

发文量

238

审稿时长

4.2 months

期刊介绍： Pesticide Biochemistry and Physiology publishes original scientific articles pertaining to the mode of action of plant protection agents such as insecticides, fungicides, herbicides, and similar compounds, including nonlethal pest control agents, biosynthesis of pheromones, hormones, and plant resistance agents. Manuscripts may include a biochemical, physiological, or molecular study for an understanding of comparative toxicology or selective toxicity of both target and nontarget organisms. Particular interest will be given to studies on the molecular biology of pest control, toxicology, and pesticide resistance. Research Areas Emphasized Include the Biochemistry and Physiology of: • Comparative toxicity • Mode of action • Pathophysiology • Plant growth regulators • Resistance • Other effects of pesticides on both parasites and hosts.