Upon infection with non-pathogenic microorganisms or treatment with natural or synthetic compounds, plants exhibit a more rapid and potent response to both biotic and abiotic stresses. However, the molecular mechanisms behind this phenomenon, known as defense priming, are poorly understood. β-aminobutyric acid (BABA) is an endogenous stress metabolite that enhances plant tolerance to various abiotic stresses and primes plant defense responses, providing the ability to resist a variety of pathogens (broad-spectrum resistance). In this study, we identified an aspartyl-tRNA synthetase (AspRS), StIBI1 (named after Arabidopsis IMPAIRED IN BABA-INDUCED IMMUNITY 1; IBI1), as a BABA receptor in Solanum tuberosum. We elucidated the regulatory mechanisms by which StIBI1 interacts with two NAC (NAM, ATAF1, 2, and CUC2) transcription factors (TFs), StVOZ1 and StVOZ2 (VASCULAR PLANT ONE ZINC FINGER, VOZ), to activate BABA-induced resistance (BABA-IR). StVOZ1 represses, whereas StVOZ2 promotes, immunity to the late blight pathogen Phytophthora infestans. Interestingly, BABA and StIBI1 influence StVOZ1- and StVOZ2-mediated immunity. StIBI1 interacts with StVOZ1 and StVOZ2 in the cytoplasm, reducing the nuclear accumulation of StVOZ1 and promoting the nuclear accumulation of StVOZ2. Our findings indicate that StVOZ1 and StVOZ2 finely regulate potato resistance to late blight through distinct signaling pathways. In summary, our study provides insights into the interaction between the potato BABA receptor StIBI1 and the TFs StVOZ1 and StVOZ2, which affects StVOZ1 and StVOZ2stability and nuclear accumulation to regulate late blight resistance during BABA-IR. This research advances our understanding of the primary mechanisms of BABA-IR in potato and contributes to a theoretical basis for the prevention and control of potato late blight using BABA-IR.

中文翻译：

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马铃薯 β-氨基丁酸受体 IBI1 操纵 VOZ1 和 VOZ2 转录因子活性以促进抗病性


在感染非病原微生物或用天然或合成化合物处理后，植物对生物和非生物胁迫表现出更快速和有效的反应。然而，这种现象背后的分子机制，被称为防御启动，知之甚少。β-氨基丁酸 （BABA） 是一种内源性胁迫代谢物，可增强植物对各种非生物胁迫的耐受性并引发植物防御反应，提供抵抗多种病原体的能力（广谱抗性）。在这项研究中，我们鉴定了一种天冬氨酰-tRNA 合成酶 （AspRS），StIBI1（以拟南芥命名 BABA 诱导免疫受损 1;IBI1） 作为马铃薯中的 BABA 受体。我们阐明了 StIBI1 与两个 NAC （NAM、ATAF1、2 和 CUC2） 转录因子 （TFs） StVOZ1 和 StVOZ2 （血管植物一个锌指，VOZ） 相互作用以激活 BABA 诱导的耐药性 （BABA-IR） 的调节机制。StVOZ1 抑制，而 StVOZ2 促进对晚期疫病病原体致病疫霉的免疫。有趣的是，BABA 和 StIBI1 影响 StVOZ1 和 StVOZ2 介导的免疫。StIBI1 与细胞质中的 StVOZ1 和 StVOZ2 相互作用，减少 StVOZ1 的核积累并促进 StVOZ2 的核积累。我们的研究结果表明，StVOZ1 和 StVOZ2 通过不同的信号通路精细调节马铃薯对晚疫病的抗性。总之，我们的研究为马铃薯 BABA 受体 StIBI1 与 TFs StVOZ1 和 StVOZ2 之间的相互作用提供了见解，这影响 StVOZ1 和 StVOZ2 的稳定性和核积累，以调节 BABA-IR 期间的晚疫病抗性。 这项研究促进了我们对马铃薯 BABA-IR 主要机制的理解，并为使用 BABA-IR 预防和控制马铃薯晚疫病提供了理论基础。