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比较转录组分析揭示了 SDHI 杀菌剂苯并呋氟草吡抑制的保守和独特机制。

Comparative Transcriptome Analyses Reveal Conserved and Distinct Mechanisms of the SDHI Fungicide Benzovindiflupyr Inhibiting .

机构信息

College of Plant Protection, Hainan University, 570228 Haikou, China.

Natural Rubber Cooperative Innovation Center of Hainan Province, Ministry of Education, China.

出版信息

Phytopathology. 2022 Jun;112(6):1255-1263. doi: 10.1094/PHYTO-10-21-0420-R. Epub 2022 Apr 24.

DOI:10.1094/PHYTO-10-21-0420-R
PMID:34879716
Abstract

Colletotrichum leaf disease (CLD) is an annual production concern for commercial growers worldwide. The succinate dehydrogenase inhibitor (SDHI) fungicide benzovindiflupyr shows higher bioactivity against CLD than other SDHIs. However, the mechanism underlying such difference remains unclear. In this study, benzovindiflupyr exhibits good inhibitory activity against and in vitro and in vivo. To reveal its mechanism for inhibiting , we compared transcriptomes of and under treatment with benzovindiflupyr and boscalid. Benzovindiflupyr exhibited higher inhibitory activity against SDH enzyme than boscalid, resulting in a greater reduction in the ATP content of isolates. Most of the metabolic pathways induced in these fungicide-treated isolates were similar, indicating that benzovindiflupyr exhibited a conserved mechanism of SDHIs inhibiting . At the same level of suppressive SDH activity, benzovindiflupyr activated more than three times greater gene numbers of than boscalid, suggesting that benzovindiflupyr could activate distinct mechanisms against . Membrane-related gene ontology terms, mainly including intrinsic components of membrane, were highly abundant for the benzovindiflupyr-treated isolates rather than boscalid-treated isolates. Only benzovindiflupyr increased the relative conductivities of hyphae, indicating that it could damage the cell membrane and increase mycelial electrolyte leakage. Thus, we proposed that the high bioactivity of benzovindiflupyr against occurred by inhibiting SDH activity and damaging the cell membrane at the same time. The research improves our understanding the mode of action of SDHI fungicides against .

摘要

炭疽叶枯病菌(CLD)是全球商业种植者每年都面临的生产问题。琥珀酸脱氢酶抑制剂(SDHI)杀菌剂苯并维氟氯吡对 CLD 的生物活性高于其他 SDHIs。然而,其差异的机制尚不清楚。在这项研究中,苯并维氟氯吡在体外和体内对 和 表现出良好的抑制活性。为了揭示其抑制 的机制,我们比较了苯并维氟氯吡和肟菌酯处理后 和 转录组。苯并维氟氯吡对 SDH 酶的抑制活性高于肟菌酯,导致 分离株的 ATP 含量降低更大。这些杀菌剂处理的分离株中诱导的大多数代谢途径相似,表明苯并维氟氯吡表现出 SDHIs 抑制 的保守机制。在抑制 SDH 活性相同的水平上,苯并维氟氯吡激活的 基因数量是肟菌酯的三倍多,表明苯并维氟氯吡可以激活针对 的不同机制。与肟菌酯处理的分离株相比,与膜相关的基因本体术语主要包括膜的内在成分,在苯并维氟氯吡处理的分离株中高度丰富。只有苯并维氟氯吡增加了菌丝的相对电导率,表明它可以破坏细胞膜并增加菌丝电解质渗漏。因此,我们提出苯并维氟氯吡对 具有高生物活性是通过同时抑制 SDH 活性和破坏细胞膜来实现的。该研究提高了我们对 SDHI 杀菌剂对 的作用模式的理解。

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