Free Radicals Mediate Systemic Acquired Resistance

Caixia Wang; Mohamed El-Shetehy; M. B. Shine; Keshun Yu; Duroy Navarre; David Wendehenne; Aardra Kachroo; Pradeep Kachroo

doi:10.1016/j.celrep.2014.03.032

Free Radicals Mediate Systemic Acquired Resistance

Caixia Wang, Mohamed El-Shetehy, M. B. Shine, Keshun Yu, Duroy Navarre, David Wendehenne, Aardra Kachroo, Pradeep Kachroo

Plant Pathology

Research output: Contribution to journal › Article › peer-review

159 Scopus citations

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.

Original language	English
Pages (from-to)	348-355
Number of pages	8
Journal	Cell Reports
Volume	7
Issue number	2
DOIs	https://doi.org/10.1016/j.celrep.2014.03.032
State	Published - Apr 24 2014

Bibliographical note

Funding 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

General Biochemistry, Genetics and Molecular Biology

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10.1016/j.celrep.2014.03.032

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title = "Free Radicals Mediate Systemic Acquired Resistance",

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.",

author = "Caixia Wang and Mohamed El-Shetehy and Shine, {M. B.} and Keshun Yu and Duroy Navarre and David Wendehenne and Aardra Kachroo and Pradeep Kachroo",

note = "Funding 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. ",

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AU - Wang, Caixia

AU - El-Shetehy, Mohamed

AU - Shine, M. B.

AU - Yu, Keshun

AU - Navarre, Duroy

AU - Wendehenne, David

AU - Kachroo, Aardra

AU - Kachroo, Pradeep

N1 - Funding 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.

PY - 2014/4/24

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N2 - 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.

AB - 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.

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Free Radicals Mediate Systemic Acquired Resistance

Abstract

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