Jasmonic acid (JA) is a crucial phytohormone that regulates plant immunity. The endogenous JA level is determined by the rates of its biosynthesis and catabolism in plants. To date, the activation of JA biosynthesis has been well documented; however, how plants repress JA catabolism upon pathogen infection remains elusive. Here, we identified Botrytis cinerea-induced F-box protein 1 (BFP1) in Arabidopsis. The expression of BFP1 was induced by B. cinerea in a JA signaling dependent manner, and BFP1 protein was critical for plant defense against B. cinerea and plant response to JA. Additionally, BFP1 overexpression increased plant defenses against broad-spectrum pathogens without fitness costs. Further experiments demonstrated that BFP1 interacts with and mediates the ubiquitination and degradation of jasmonic acid oxidases (JAOs, also known as jasmonate-induced oxygenases, JOXs), the enzymes that hydroxylate JA to 12OH-JA. Consistently, the accumulation of JA and 12OH-JA was regulated by BFP1 during B. cinerea infection. Moreover, mutation of JAO2 complemented the phenotypic effects of the bfp1 mutant. Collectively, our results unveil an undiscovered strategy to enhance plant immunity by suppressing the catabolism of immune-related hormone.

茉莉酸（JA）是调节植物免疫力的重要植物激素。内源性 JA 水平由其在植物中的生物合成和分解代谢速率决定。迄今为止，JA 生物合成的激活已得到充分记录。然而，植物如何在病原体感染时抑制 JA 分解代谢仍然难以捉摸。在这里，我们在拟南芥中鉴定了灰葡萄孢诱导的 F-box 蛋白 1 (BFP1)。BFP1的表达是由B. cinerea以 JA 信号依赖方式诱导的，并且 BFP1 蛋白对于植物针对B. cinerea 的防御和植物对 JA 的反应至关重要。此外，BFP1过度表达增强了植物对广谱病原体的防御能力，且无需付出健康代价。进一步的实验表明，BFP1 与茉莉酸氧化酶（JAO，也称为茉莉酸诱导加氧酶，JOX）相互作用并介导其泛素化和降解，茉莉酸氧化酶将 JA 羟基化为 12OH-JA。一致地，在B. cinerea感染期间，JA 和 12OH-JA 的积累受到 BFP1 的调节。此外，JAO2的突变补充了bfp1突变体的表型效应。总的来说，我们的结果揭示了一种未被发现的策略，通过抑制免疫相关激素的分解代谢来增强植物免疫力。