The Arabidopsis thaliana Calmodulin-binding Transcription Activator (CAMTA) transcription factors CAMTA1, CAMTA2, and CAMTA3 (CAMTA123) serve as master regulators of salicylic acid (SA)-mediated immunity, repressing the biosynthesis of SA in healthy plants. Here, we show that CAMTA123 also repress the biosynthesis of pipecolic acid (Pip) in healthy plants. Loss of CAMTA123 function resulted in the induction of AGD2-like defense response protein 1 (ALD1), which encodes an enzyme involved in Pip biosynthesis. Induction of ALD1 resulted in the accumulation of high levels of Pip, which brought about increased levels of the SA receptor protein NPR1 without induction of NPR1 expression or requirement for an increase in SA levels. Pip-mediated induction of ALD1 and genes regulating the biosynthesis of SA—CBP60g, SARD1, PAD4, and EDS1—was largely dependent on NPR1. Furthermore, Pip-mediated increase in NPR1 protein levels was associated with priming of Pip and SA biosynthesis genes to induction by low levels of SA. Taken together, our findings expand the role for CAMTA123 in regulating key immunity genes and suggest a working model whereby loss of CAMTA123 repression leads to the induction of plant defense genes and initiation of SAR.

在拟南芥钙调蛋白-结合转录激活剂（CAMTA）转录因子CAMTA1，CAMTA2，和CAMTA3（CAMTA123）作为水杨酸（SA）介导的免疫力的主调节剂，抑制SA的生物合成在健康的植物。在这里，我们表明CAMTA123还可以抑制健康植物中胡椒酸（Pip）的生物合成。CAMTA123功能的丧失导致了AGD2样防御反应蛋白1（ALD1）的诱导，该蛋白编码参与Pip生物合成的酶。ALD1的诱导导致高水平Pip的积累，从而导致SA受体蛋白NPR1的水平增加而没有诱导NPR1表达或要求增加SA水平。PIP介导的诱导ALD1和基因调节SA-生物合成CBP60g，SARD1，PAD4和EDS1 -was很大程度上依赖于NPR1。此外，Pip介导的NPR1蛋白水平增加与Pip和SA生物合成基因引发低水平SA诱导有关。综上所述，我们的发现扩大了CAMTA123在调节关键免疫基因中的作用，并提出了一种工作模型，其中CAMTA123阻遏作用的丧失导致了植物防御基因的诱导和SAR的启动。