The target site of the novel fungicide quinofumelin, Pyricularia oryzae class II dihydroorotate dehydrogenase.

IF 1.5 4区 农林科学 Q2 ENTOMOLOGY Journal of Pesticide Science Pub Date : 2022-11-20 DOI:10.1584/jpestics.D22-027
Norikazu Higashimura, Akira Hamada, Toshiaki Ohara, Seiya Sakurai, Hiroyuki Ito, Shinichi Banba
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引用次数: 2

Abstract

The target site of the novel fungicide quinofumelin was investigated in the rice blast fungus Pyricularia oryzae. Quinofumelin-induced mycelial growth inhibition was reversed by orotate but not by dihydroorotate. Recovery tests suggested that the target site of quinofumelin was dihydroorotate dehydrogenase (DHODH), which catalyzes the oxidation of dihydroorotate to orotate. Quinofumelin strongly inhibited P. oryzae class 2 DHODH (DHODH II) (IC50: 2.8 nM). The inhibitory activities of mycelial growth and DHODH II were strongly positively correlated, indicating that DHODH II inhibition by quinofumelin lead to antifungal activity. A P. oryzae DHODH II gene (PoPYR4) disruption mutant (ΔPopyr4), showing the same tendency as the quinofumelin-treated wild strain in recovery tests, was constructed, and disease symptoms were not observed in rice plants infected by ΔPopyr4. Thus, DHODH II, which plays an important role in pathogenicity and mycelial growth, is found to be the target site of quinofumelin.

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新型杀菌剂喹诺菲林ⅱ类二氢根酸脱氢酶的靶点。
研究了新型杀菌剂喹啉在稻瘟病菌中的作用位点。喹诺菲美林诱导的菌丝生长抑制被旋甲酸逆转,而非二氢旋甲酸逆转。回收率试验表明,喹诺菲林的靶点是二氢甲酯脱氢酶(DHODH),该酶催化二氢甲酯氧化生成甲酯。喹诺菲林对P. oryzae 2类DHODH (DHODH II)有较强的抑制作用(IC50: 2.8 nM)。菌丝生长抑制活性与DHODH II呈强正相关,表明喹诺菲林抑制DHODH II具有抗真菌活性。构建了一个稻瘟病菌DHODH II基因(PoPYR4)破坏突变体(ΔPopyr4),在恢复试验中表现出与喹诺芬林处理的野生菌株相同的趋势,并且在感染ΔPopyr4的水稻植株中未观察到疾病症状。因此,发现在致病性和菌丝生长中起重要作用的DHODH II是喹诺芬林的靶点。
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来源期刊
Journal of Pesticide Science
Journal of Pesticide Science 农林科学-昆虫学
CiteScore
4.30
自引率
4.20%
发文量
28
审稿时长
18-36 weeks
期刊介绍: The Journal of Pesticide Science publishes the results of original research regarding the chemistry and biochemistry of pesticides including bio-based materials. It also covers their metabolism, toxicology, environmental fate and formulation.
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