The IBI1 Receptor of β-Aminobutyric Acid Interacts with VOZ Transcription Factors to Regulate Abscisic Acid Signaling and Callose-Associated Defense

External and internal signals can prime the plant immune system for a faster and/or stronger response to pathogen attack. beta-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 (BABAIR), 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.