Zhang Ziyang, Song Xinhao, Qiu Hui, Guo Yu, Xu Chao, Zhang Haibo, Cai Yiqiang, Zhang Jie, Zhu Feng, Yang Hongfu, Tian Zihua, Zhang Shuai, Zhou Mingguo, Duan Yabing
State Key Laboratory of Agricultural and Forestry Biosecurity, College of Plant Protection, Nanjing Agricultural University, Nanjing 210095, China.
Jiangsu Hilly Area Zhenjiang Institute of Agricultural Sciences, Jiangsu Academy of Agricultural Sciences, Jurong 212400, China.
Pestic Biochem Physiol. 2025 Sep;213:106482. doi: 10.1016/j.pestbp.2025.106482. Epub 2025 May 30.
Fusarium head blight (FHB), primarily caused by the Fusarium graminearum species complex (FGSC), is a devastating fungal disease that threatens global wheat production and endangers worldwide food security. Phenamacril, a myosin5 inhibitor, is widely recognized as an effective fungicide against FGSC. Since 2007, phenamacril has been registered in China for the control of FHB. While the resistance mechanisms in laboratory-induced phenamacril-resistant mutants of FGSC have been documented, the field resistance mechanisms remain poorly understood. In this study, we identified six F. asiaticum isolates with high resistance to phenamacril from a collection of 5163 FGSC isolates. Sequence alignment analysis revealed these resistant isolates harbor an E420K point mutation in myosin5. Site-directed mutagenesis experiments confirmed that the E420K mutation in myosin5 confers high resistance to phenamacril in F. asiaticum. No cross-resistance was observed between phenamacril and pyraclostrobin, pydiflumetofen, or tebuconazole. Additionally, the mycelial growth, spore production, and pathogenicity of phenamacril-resistant isolates were diminished, indicating a reduced fitness of these resistant isolates. Molecular docking results further indicated that the E420K mutation in FaMyosin5 decreases its binding affinity for phenamacril compared to the wild-type FaMyosin5. Collectively, this study provides the first evidence that E420K mutation in myosin5 confers field resistance to phenamacril in F. asiaticum. These findings provide critical insights for monitoring and managing phenamacril resistance in FGSC.
小麦赤霉病（FHB）主要由禾谷镰刀菌物种复合体（FGSC）引起，是一种毁灭性的真菌病害，威胁着全球小麦生产并危及全球粮食安全。苯噻酰胺是一种肌球蛋白5抑制剂，被广泛认为是一种针对FGSC的有效杀菌剂。自2007年以来，苯噻酰胺已在中国登记用于防治小麦赤霉病。虽然在实验室诱导的FGSC苯噻酰胺抗性突变体中的抗性机制已有记录，但田间抗性机制仍知之甚少。在本研究中，我们从5163个FGSC分离株中鉴定出6个对苯噻酰胺具有高抗性的亚洲镰刀菌分离株。序列比对分析显示，这些抗性分离株在肌球蛋白5中存在E420K点突变。定点诱变实验证实，肌球蛋白5中的E420K突变赋予亚洲镰刀菌对苯噻酰胺的高抗性。未观察到苯噻酰胺与唑菌酯、氟吡菌酰胺或戊唑醇之间的交叉抗性。此外，苯噻酰胺抗性分离株的菌丝生长、孢子产生和致病性均降低，表明这些抗性分离株的适合度降低。分子对接结果进一步表明，与野生型Fa肌球蛋白5相比，Fa肌球蛋白5中的E420K突变降低了其与苯噻酰胺的结合亲和力。总的来说，本研究提供了首个证据，即肌球蛋白5中的E420K突变赋予亚洲镰刀菌对苯噻酰胺的田间抗性。这些发现为监测和管理FGSC中的苯噻酰胺抗性提供了关键见解。
