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S-Nitrosoglutathione Reductase-Modulated Redox Signaling Controls Sodic Alkaline Stress Responses in Solanum lycopersicum L.
Author(s) -
Biao Gong,
Dan Wen,
Xiufeng Wang,
Min Wei,
Fengjuan Yang,
Yan Li,
Qinghua Shi
Publication year - 2014
Publication title -
plant and cell physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.975
H-Index - 152
eISSN - 1471-9053
pISSN - 0032-0781
DOI - 10.1093/pcp/pcv007
Subject(s) - reactive oxygen species , nitric oxide , reactive nitrogen species , oxidative stress , chemistry , homeostasis , microbiology and biotechnology , reductase , biochemistry , abiotic stress , signal transduction , biology , enzyme , gene , organic chemistry
S-Nitrosoglutathione reductase (GSNOR) plays an important role in regulating nitric oxide (NO) and S-nitrosothiol (SNO) homeostasis, and is therefore involved in the modulation of processes mediated by reactive nitrogen species (RNS). Although RNS have emerged as a key component in plant response to abiotic stress, knowledge of their regulation by GSNOR under alkaline stress was lacking. In this study, metabolic regulation of NO and SNOs was investigated in tomato plants of the wild type (WT), GSNOR overexpression lines (OE-1/2) and GSNOR suppression lines (AS-1/2) grown under either control conditions or sodic alkaline stress. Phenotype, photosynthesis, reactive oxygen species (ROS) metabolism, Na(+)-K(+) homeostasis and expression of genes encoding ROS scavenging, Na(+) detoxification and programmed cell death (PCD) were also analyzed. Compared with WT lines, OE-1/2 lines were alkaline tolerant, while AS-1/2 lines were alkaline sensitive. In AS-1/2 lines, although genetic expression of Na(+) detoxification was activated by GSNOR-regulated NO and ROS signaling, excess RNS and ROS accumulation also led to serious oxidative stress and induced PCD. In contrast, overexpression of GSNOR significantly increased ROS scavenging efficiency. Thus, it seemed that increasing alkaline tolerance via GSNOR overexpression in tomato was attributed to the regulation of redox signaling including RNS and ROS.

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