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Cell Rep. 2014 Apr 24;7(2):348-355. doi: 10.1016/j.celrep.2014.03.032. Epub 2014 Apr 13.

Free radicals mediate systemic acquired resistance.

Author information

1
College of Agronomy and Plant Protection, Qingdao Agricultural University, Qingdao 266109, P.R. China; Department of Plant Pathology, University of Kentucky, Lexington, KY 40546, USA.
2
Department of Plant Pathology, University of Kentucky, Lexington, KY 40546, USA.
3
U.S. Department of Agriculture - Agricultural Research Service, Washington State University, Prosser, WA 99350, USA.
4
Université de Bourgogne, ERL CNRS 6300, UMR 1347 Agroécologie, BP 86510, 21065 Dijon, France.
5
Department of Plant Pathology, University of Kentucky, Lexington, KY 40546, USA. Electronic address: pk62@uky.edu.

Abstract

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.

PMID:
24726369
DOI:
10.1016/j.celrep.2014.03.032
[Indexed for MEDLINE]
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