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线粒体相关蛋白 FgNdk1 通过与琥珀酸脱氢酶相互作用调控 的发育、致病性和 SDHI 杀菌剂敏感性。

Mitochondria-Associated Protein FgNdk1 Regulates the Development, Pathogenicity, and SDHI Fungicide Sensitivity of by Interacting with Succinate Dehydrogenase.

机构信息

College of Plant Protection, Nanjing Agricultural University, Nanjing 210095, Jiangsu, China.

出版信息

J Agric Food Chem. 2024 Feb 28;72(8):3913-3925. doi: 10.1021/acs.jafc.3c07934. Epub 2024 Feb 14.

DOI:10.1021/acs.jafc.3c07934
PMID:38355300
Abstract

Nucleoside diphosphate kinase (NDK) plays an important role in many cellular processes in all organisms. In this study, we functionally characterized a nucleoside diphosphate kinase (FgNdk1) in , a causal agent of Fusarium head blight (FHB). FgNdk1 was involved in the generation of energy in the electron-transfer chain by interacting with succinate dehydrogenase (FgSdhA, FgSdhC, and FgSdhC). Deletion of not only resulted in abnormal mitochondrial morphology, decreased ATP content, defective fungal development, and impairment in the formation of the toxisome but also led to the suppressed expression level of DON biosynthesis enzymes, decreased DON biosynthesis, and declined pathogenicity as well. Furthermore, deletion of caused increasing transcriptional levels of and , in the presence of pydiflumetofen, related to the decreased sensitivity to SDHI fungicides. Overall, this study identified a new regulatory mechanism of FgNdk1 in the pathogenicity and SDHI fungicide sensitivity of .

摘要

核苷二磷酸激酶(NDK)在所有生物体的许多细胞过程中都起着重要作用。在这项研究中,我们对镰刀菌穗腐病菌(Fusarium head blight,FHB)的致病因子 中的核苷二磷酸激酶(FgNdk1)进行了功能表征。FgNdk1 通过与琥珀酸脱氢酶(FgSdhA、FgSdhC 和 FgSdhC)相互作用,参与电子传递链中的能量产生。缺失不仅导致线粒体形态异常、ATP 含量降低、真菌发育缺陷以及毒素体形成受损,还导致 DON 生物合成酶的表达水平受到抑制、DON 生物合成减少以及致病性降低。此外,缺失导致 pydiflumetofen 存在时 和 的转录水平增加,与对 SDHI 杀菌剂敏感性降低有关。总的来说,这项研究鉴定了 FgNdk1 在 的致病性和 SDHI 杀菌剂敏感性中的一个新的调控机制。

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