Summary: Systemic acquired resistance (SAR) is a form of resistance that protects plants against a broad spectrum of secondary infections. However, exploiting SAR for the protection of agriculturally important plants warrants a thorough investigation of the mutual interrelationships among the various signals that mediate SAR. Here, we show that nitric oxide (NO) and reactive oxygen species (ROS) serve as inducers of SAR in a concentration-dependent manner. Thus, genetic mutations that either inhibit NO/ROS production or increase NO accumulation (e.g., a mutation in S-nitrosoglutathione reductase [GSNOR]) abrogate SAR. Different ROS function additively to generate the fatty-acid-derived azelaic acid (AzA), which in turn induces production of the SAR inducer glycerol-3-phosphate (G3P). Notably, this NO/ROS→AzA→G3P-induced signaling functions in parallel with salicylic acid-derived signaling. We propose that the parallel operation of NO/ROS and SA pathways facilitates coordinated regulation in order to ensure optimal induction of SAR. : Nitric oxide (NO) and reactive oxygen species (ROS) serve as signaling molecules in diverse organisms. Here, Wang et al. show that NO and ROS also serve as inducers of systemic acquired resistance (SAR), an important form of broad-spectrum immunity in plants. Their results suggest that NO and ROS act in a concentration-dependent manner and in parallel with salicylic-acid-derived signaling to induce SAR. NO and ROS act as upstream signals in the pathway that includes azelaic acid, glycerol-3-phosphate, and the lipid-transfer-like proteins DIR1/AZI1.
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