In this study, we used virus-mediated gene silencing technology and found that the HSP17.4 gene-silenced cultivar Sweet Charlie plants were more susceptible to Colletotrichum gloeosporioides than the wild-type Sweet Charlie, and the level of infection was even higher than that of the susceptible cultivar Benihopp. The results of differential quantitative proteomics showed that after infection with the pathogen, the expression of the downstream response genes NPR1, TGA, and PR-1 of the salicylic acid (SA) signalling pathway was fully up-regulated in the wild-type Sweet Charlie, and the expression of the core transcription factor MYC2 of the jasmonic acid (JA) pathway was significantly down-regulated. The expression of the proteins encoded by these genes did not change significantly in the HSP17.4-silenced Sweet Charlie, indicating that the expression of HSP17.4 activated the up-regulation of downstream signals of SA and inhibited the JA signal pathway. The experiments that used SA, methyl jasmonate, and their inhibitors to treat plants provide additional evidence that the antagonism between SA and JA regulates the resistance of strawberry plants to C. gloeosporioides.

中文翻译：

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HSP17.4介导水杨酸和茉莉酸途径调节草莓对胶孢炭疽病菌的抗性

本研究采用病毒介导的基因沉默技术，发现HSP17.4基因沉默的栽培品种甜查理植物比野生型甜查理更易感染胶孢炭疽病菌，感染程度甚至高于野生型甜查理。易感品种 Benihopp。差异定量蛋白质组学结果表明，病原体感染后，下游反应基因NPR1、TGA、PR-1的表达水杨酸（SA）信号通路在野生型 Sweet Charlie 中完全上调，茉莉酸（JA）通路核心转录因子 MYC2 的表达显着下调。这些基因编码的蛋白质在HSP17.4沉默的Sweet Charlie中的表达没有显着变化，表明HSP17.4的表达激活了SA下游信号的上调并抑制了JA信号通路。使用 SA、茉莉酸甲酯及其抑制剂处理植物的实验提供了额外的证据，表明 SA 和 JA 之间的拮抗作用调节了草莓植物对C的抗性。球孢子菌。