Xueqiong Xiao / University of Kenctuky; Huazhong Agricultural University
Ruiying Liu / University of Kentucky
Keshun Yu / University of Kentucky
Aardra Kachroo / University of Kentucky
Pradeep Kachroo / University of Kentucky
Systemic acquired resistance (SAR) is initiated by a plant upon recognition of microbial effectors, involves generation of mobile signals at the primary infection site (local), which translocate to and activate defense responses in uninfected (distal) tissues, resulting in broad-spectrum resistance against pathogens. Our previous studies suggested that nitric oxide (NO)⇔oxygen species (ROS)⇒azelaic acid (AzA)⇒glycerol-3-phosphate (G3P) signaling functions in parallel with salicylic acid (SA)-mediated signaling to induce SAR. Pipecolic acid (Pip), is a non-proteinaceous product of lysine catabolism, and exogenous application of Pip confers SAR. To better understand the role of Pip in SAR, we investigated its relationship with SA- and NO-ROS-G3P-mediated pathways. Our results show that Pip confers SAR by increasing levels of NO, ROS, and G3P, but not SA. A defect in Pip biosynthesis in ald1 plants impairs accumulation of ROS, AzA, and G3P but not SA. Thus, Pip-mediated SAR is dependent on the NO/ROS-G3P branch of the SAR pathway, and Pip functions primarily upstream of the NO⇔ROS⇒AzA⇒G3P pathway. However, plants defective in G3P or SA biosynthesis accumulate reduced levels of Pip in their distal uninfected tissues although they contain wild-type-like levels of Pip in their infected leaves. These data indicate that de novo synthesis of Pip in distal tissues is dependent on both SA and G3P and the distal levels of SA and G3P play an important role in SAR.