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枯萎病菌(Fusarium oxysporum f. sp. melonis)对肌球蛋白抑制剂苯霜灵的抗药性风险评估。

Resistance risk assessment of Fusarium oxysporum f. sp. melonis against phenamacril, a myosin inhibitor.

机构信息

College of Plant Protection, Nanjing Agricultural University, Key Laboratory of Pesticide, Jiangsu Province, Nanjing 210095, China.

College of Plant Protection, Nanjing Agricultural University, Key Laboratory of Pesticide, Jiangsu Province, Nanjing 210095, China.

出版信息

Pestic Biochem Physiol. 2018 May;147:127-132. doi: 10.1016/j.pestbp.2017.09.014. Epub 2017 Oct 7.

DOI:10.1016/j.pestbp.2017.09.014
PMID:29933982
Abstract

Fusarium wilt caused by Fusarium oxysporum f. sp. melonis (FOM) is one of the most notorious seed-borne diseases worldwide. Phenamacril is a cyanoacrylate fungicide with novel chemical structure and strong inhibitive activity against FOM. To evaluate the risk of FOM developing phenamacril resistance, five phenamacril-resistant mutants with >800μgml minimum inhibitory concentration were obtained by repeated exposure to the fungicide in the laboratory. Compared with the parental isolate, four of the five phenamacril-resistant mutants showed enhanced biological fitness in sporulation and virulence, but not in sensitivity to various stresses (oxidative and osmotic pressure, cell membrane and wall inhibitor). No positive cross-resistance was observed among phenamacril and the other five fungicides, including azoxystrobin, carbendazim, boscalid, fluazinam and tebuconazole. Sequencing alignment results of the myosin 5 from the five resistant mutants and the parental strain indicated that the three resistant mutants fo-2, fo-3 and fo-4 had a single point mutation (S175L), which may confer the resistance of FOM against phenamacril. Interestingly, the resistant mutant fo-4 harbored not only one mutation (S175L) at myosin 5, but also the other mutation (A52G) at β-tublin. Our data supported that resistance risk of Fusarium oxysporum f. sp. melonis against phenamacril was between the moderate to high level.

摘要

镰刀菌枯萎病由尖孢镰刀菌西瓜专化型(Fusarium oxysporum f. sp. melonis,FOM)引起,是全球最著名的种传病害之一。苯霜灵是一种具有新颖化学结构的氰基丙烯酸酯类杀菌剂,对 FOM 具有强烈的抑制活性。为了评估 FOM 产生苯霜灵抗性的风险,通过在实验室中反复接触杀菌剂,获得了 5 株具有 >800μgml 最小抑菌浓度的苯霜灵抗性突变体。与亲本分离株相比,这 5 株苯霜灵抗性突变体中的 4 株在产孢和致病力方面表现出增强的生物适应性,但对各种胁迫(氧化和渗透压、细胞膜和细胞壁抑制剂)的敏感性没有变化。在苯霜灵和其他五种杀菌剂(包括肟菌酯、多菌灵、啶酰菌胺、氟唑菌酰胺和戊唑醇)之间没有观察到正交叉抗性。对来自五个抗性突变体和亲本菌株的肌球蛋白 5 的测序比对结果表明,三个抗性突变体 fo-2、fo-3 和 fo-4 具有一个单点突变(S175L),这可能导致 FOM 对苯霜灵产生抗性。有趣的是,抗性突变体 fo-4 不仅在肌球蛋白 5 上具有一个突变(S175L),而且在β-微管蛋白上还具有另一个突变(A52G)。我们的数据表明,尖孢镰刀菌西瓜专化型对苯霜灵的抗性风险处于中等到高度水平之间。

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