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The Discovery of Oxathiapiprolin as a Potential Agent for the Control of Litchi Downy Blight Caused by Peronophythora litchii and the Study of Its Mechanism of Action
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2024-12-16 , DOI: 10.1021/acs.jafc.4c09639
Sirui Cheng, Kezhu Tao, Xin Lv, Zhenduo Lai, Yi Lv, Zhixin Wang, Qinghe Chen

Oxathiapiprolin, a novel fungicide targeting oxysterol-binding proteins (OSBP), has proven to be effective against various oomycete diseases, but its effects on pathogens remain underexplored. In this study, we demonstrated that oxathiapiprolin inhibits mycelium growth, sporangium production, zoospore release, and oospore production in Peronophythora litchii, with 50% effective concentrations ranging from 0.000153 to 0.011681 μg mL–1. Additionally, in vivo tests confirmed its efficacy in controlling litchi downy blight. Our study demonstrated that oxathiapiprolin disrupts cellular ultrastructure and plasma membrane integrity, affects stress sensitivity, inhibits sterol transport, increases autophagy levels, reduces lipid droplet content, and induces lipid metabolism disorders. Gene expression analysis revealed that oxathiapiprolin affects the expression of PlORP1 (ORP1 gene of P. litchii), with docking simulations further confirming its interaction with the PlORP1 (ORP1 protein of P. litchii) protein. Ultimately, this cascade of events led to pathogen death. This paper reveals the antioomycete mechanism of oxathiapiprolin against P. litchii.

中文翻译:


发现 Oxathiapiprolin 作为控制 Peronophythora litchii 引起的荔枝霜枯病的潜在药物及其作用机制的研究



Oxathiapiprolin 是一种靶向氧甾醇结合蛋白 (OSBP) 的新型杀菌剂,已被证明对各种卵菌疾病有效,但其对病原体的影响仍未得到充分探索。在这项研究中,我们证明了 oxathiapiprolin 抑制荔枝 Peronophythora litchii 的菌丝体生长、孢子囊产生、游动孢子释放和卵孢子产生,50% 有效浓度范围为 0.000153 至 0.011681 μg mL-1。此外,体内试验证实了其控制荔枝霜枯病的功效。我们的研究表明,氧噻哌普林破坏细胞超微结构和质膜完整性,影响应激敏感性,抑制甾醇转运,增加自噬水平,降低脂滴含量,并诱导脂质代谢紊乱。基因表达分析显示,氧噻哌哌素影响 PlORP1P. litchii 的 ORP1 基因) 的表达,对接模拟进一步证实了它与 PlORP1 (P. litchii 的 ORP1 蛋白) 蛋白的相互作用。最终,这一系列事件导致了病原体的死亡。本文揭示了 oxathiapiprolin 对抗 P. litchii 的抗卵菌机制。
更新日期:2024-12-17
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