Pipecolic acid confers systemic immunity by regulating free radicals

Area of Science:

• Plant immunity
• Molecular signaling
• Metabolite biosynthesis

Background:

• Pipecolic acid (Pip), a lysine catabolism product, regulates immunity in plants and humans.
• Pip accumulates during pathogen infection and is linked to systemic acquired resistance (SAR).
• Molecular mechanisms of Pip-mediated signaling and its relation to other SAR inducers are unclear.

Purpose of the Study:

• To elucidate the molecular mechanisms of Pip-mediated SAR in plants.
• To investigate the relationship between Pip, nitric oxide (NO), reactive oxygen species (ROS), glycerol-3-phosphate (G3P), and salicylic acid (SA) in plant immunity.

Main Methods:

• Analysis of Pip accumulation in wild-type and mutant plants (defective in NO, ROS, G3P, or SA biosynthesis) upon pathogen infection.
• Measurement of NO, ROS, G3P, and SA levels in infected and distal uninfected tissues.

Main Results:

• Pip confers SAR by increasing NO and ROS levels, which act upstream of G3P.
• Plants with defects in NO, ROS, G3P, or SA biosynthesis show reduced Pip accumulation in distal tissues.
• De novo Pip synthesis in distal tissues is dependent on SA and G3P, highlighting their role in SAR.

Conclusions:

• Pip-mediated SAR involves a signaling cascade where NO and ROS increase upstream of G3P.
• SA and G3P are essential for de novo Pip synthesis in distal tissues, playing a critical role in SAR.
• Metabolites within the signaling cascade can mutually stimulate their biosynthesis based on levels and location.