Two signal molecules, salicylic acid (SA) and N-hydroxypipecolic acid (NHP), play critical roles in plant immunity. The biosynthetic genes of both compounds are positively regulated by master immune-regulating transcription factors SARD1 and CBP60g. However, the relationship between the SA and NHP pathways is unclear. CALMODULIN-BINDING TRANSCRIPTION FACTOR 1 (CAMTA1), CAMTA2, and CAMTA3 are known redundant negative regulators of plant immunity, but the underlying mechanism also remains largely unknown. In this study, through chromatin immunoprecipitation and electrophoretic mobility shift assays, we uncovered that CBP60g is a direct target of CAMTA3, which also negatively regulates the expression of SARD1, presumably via an indirect effect. The autoimmunity of camta3-1 is suppressed by sard1 cbp60g double mutant as well as ald1 and fmo1, two single mutants defective in NHP biosynthesis. Interestingly, a suppressor screen conducted in the camta1/2/3 triple mutant background yielded various mutants blocking biosynthesis or signaling of either SA or NHP, leading to nearly complete suppression of the extreme autoimmunity of camta1/2/3, suggesting that the SA and NHP pathways can mutually amplify each other. Together, these results reveal that CAMTAs repress the biosynthesis of SA and NHP by modulating the expression of SARD1 and CBP60g, and that the SA and NHP pathways are coordinated to optimize plant immune response.

水杨酸（SA）和N-羟基哌酸（NHP）这两个信号分子在植物免疫中起关键作用。两种化合物的生物合成基因均受主要的免疫调节转录因子SARD1和CBP60g的正调节。但是，SA和NHP途径之间的关系尚不清楚。钙调蛋白结合转录因子1（CAMTA1），CAMTA2和CAMTA3是已知的植物免疫冗余负调节剂，但其潜在机理也仍然未知。在这项研究中，通过染色质免疫沉淀和电泳迁移率变动分析，我们发现CBP60g是CAMTA3的直接靶标，它也负调节SARD1的表达，可能是间接作用。的自身免疫camta3-1通过抑制sard1 cbp60g双重突变体以及ALD1和FMO1，两个单突变体中生物合成NHP有缺陷。有趣的是，在进行了抑制屏幕camta1 / 2 / 3三重突变体背景产生各种突变体阻断生物合成或任一SA或NHP的信令，导致的极端自身免疫几乎完全抑制camta1 / 2 / 3，表明SA和NHP途径可以相互放大。总之，这些结果表明，CAMTA通过调节SARD1和CBP60g的表达来抑制SA和NHP的生物合成，并且SA和NHP途径相互配合以优化植物的免疫反应。