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.
|Number of pages||8|
|State||Published - Apr 24 2014|
Bibliographical noteFunding Information:
This work was supported by grants from the National Science Foundation (MCB-0421914 and IOS-051909) and the United Soybean Board (1244). M.E.-S. was supported by a fellowship from the Egyptian government. We thank Joanne Holden for help with SA estimations, Guillaume Robin for help with images, Gah-Hyun Lim for help with NO estimations, Evan Stearns for help with expression analysis, Anne-Frances Miller for help with EPR analysis, and Ludmila Lapchyk and Amy Crume for technical support. We thank Nigel Crawford for noa1 , Dan Klessig for bsmt1 , Zhen-Ming Pei for nox1 , Miguel Angel Torres and Jeff Dangl for rbohD and rbohF , and the Arabidopsis Biological Resource Center for nia1 , nia2 , and gsnor1 seeds.
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology (all)