External and internal signals can prime the plant immune system for a faster and/or stronger response to pathogen attack. β-aminobutyric acid (BABA) is an endogenous stress metabolite that induces broad-spectrum disease resistance in plants. BABA perception in Arabidopsis is mediated by the aspartyl tRNA synthetase IBI1, which activates priming of multiple immune responses, including callose-associated cell wall defenses that are under control by abscisic acid (ABA). However, the immediate signaling components after BABA perception by IBI1, as well as the regulatory role of ABA therein, remain unknown. Here, we have studied the early signaling events controlling IBI1-dependent BABA-induced resistance (BABA-IR), using untargeted transcriptome and protein interaction analyses. Transcriptome analysis revealed that IBI1-dependent expression of BABA-IR against the biotrophic oomycete Hyaloperonospora arabidopsidis is associated with suppression of ABA-inducible abiotic stress genes. Protein interaction studies identified the VOZ1 and VOZ2 transcription factors (TFs) as IBI1-interacting partners, which are transcriptionally induced by ABA but suppress pathogen-induced expression of ABA-dependent genes. Furthermore, we show that VOZ TFs require nuclear localization for their contribution to BABA-IR by mediating augmented expression of callose-associated defense. Collectively, our study indicates that the IBI1-VOZ signaling module channels pathogen-induced ABA signaling toward cell wall defense while simultaneously suppressing abiotic stress-responsive genes.

外部和内部信号可以使植物免疫系统对病原体攻击做出更快和/或更强的反应。β-氨基丁酸 (BABA) 是一种内源性胁迫代谢物，可诱导植物的广谱抗病性。拟南芥中的BABA 感知由天冬氨酰 tRNA 合成酶 IBI1 介导，IBI1 可激活多种免疫反应，包括受脱落酸 (ABA) 控制的胼胝相关细胞壁防御。然而，IBI1 感知 BABA 后的即时信号成分，以及 ABA 在其中的调节作用，仍然未知。在这里，我们使用非靶向转录组和蛋白质相互作用分析研究了控制 IBI1 依赖性 BABA 诱导的抗性 (BABA-IR) 的早期信号事件。转录组分析显示，BABA-IR 的 IBI1 依赖性表达对生物营养型卵菌Hyaloperonospora arabidopsidis与抑制 ABA 诱导的非生物胁迫基因有关。蛋白质相互作用研究将 VOZ1 和 VOZ2 转录因子 (TF) 鉴定为 IBI1 相互作用伙伴，它们由 ABA 转录诱导，但抑制病原体诱导的 ABA 依赖性基因的表达。此外，我们表明 VOZ TF 需要核定位才能通过介导胼胝相关防御的增强表达来对 BABA-IR 做出贡献。总的来说，我们的研究表明 IBI1-VOZ 信号模块将病原体诱导的 ABA 信号传导至细胞壁防御，同时抑制非生物应激反应基因。