Scholarlink

<p>High salt stress can hinder plant growth and development, thus reducing crop yield and quality. As an important signaling molecule, NO is involved in regulating various physiological and biochemical processes in plants. In this study, tobacco seedlings treated with 200 mmol/L NaCl exhibited leaf etiolation, sharp increases in superoxide anion (O<sub>2</sub><sup>−</sup>) and peroxynitrite anion (ONOO<sup>−</sup>) contents, reduced activities of photosystem I (PSI) and II (PSII) reaction centers, and obstructed electron transfer. However, overexpression of the gene encoding the NO regulator nitrosoglutathione reductase (GSNOR) reduced the excessive accumulation of nitric oxide (NO) and <i>S</i>-nitrosothiol (GSNO) during NaCl stress. It also enhanced antioxidant enzyme activity and the contents of antioxidant substances, thereby maintaining the homeostasis of reactive oxygen species and reactive nitrogen species. Moreover, GSNOR also promoted photosynthesis in tobacco leaves at the transcriptional level. Through enrichment analysis of differentially expressed genes (DEGs) and weighted gene co-expression network analysis (WGCNA) based on physiological and RNA-seq data, it was found that photosynthesis-related pathways, including “Porphyrin and chlorophyll metabolism”, “Carbon fixation in photosynthetic organisms,” and “Photosynthesis,” were significantly enriched. In <i>GSNOR</i>-overexpression plants, the expression of genes encoding proteins involved in chlorophyll synthesis, the Calvin cycle, PSII, and PSI were upregulated. Meanwhile, leaf chlorophyll increased, and the net photosynthetic rate, stomatal conductance, and activity of the reaction centers were enhanced. In contrast, <i>GSNOR</i>-inhibited plants exhibited the opposite trends. These results indicate that NO enhances the salt tolerance of tobacco seedlings by promoting photosynthesis and enhancing antioxidant capacity.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

GSNOR mediates NO signaling to enhance salt tolerance in tobacco by regulating redox and photosynthesis

  • 期刊论文

  • 发表日期：

    2026年3月13日

查看全文
  • Yu Zhang,
  • Yixuan Feng,
  • Yanjie Liu,
  • Yongzheng Qiu,
  • Xiaoyu Zhang,
  • Jieyun Cheng,
  • Yue Wang

摘要

High salt stress can hinder plant growth and development, thus reducing crop yield and quality. As an important signaling molecule, NO is involved in regulating various physiological and biochemical processes in plants. In this study, tobacco seedlings treated with 200 mmol/L NaCl exhibited leaf etiolation, sharp increases in superoxide anion (O2−) and peroxynitrite anion (ONOO−) contents, reduced activities of photosystem I (PSI) and II (PSII) reaction centers, and obstructed electron transfer. However, overexpression of the gene encoding the NO regulator nitrosoglutathione reductase (GSNOR) reduced the excessive accumulation of nitric oxide (NO) and S-nitrosothiol (GSNO) during NaCl stress. It also enhanced antioxidant enzyme activity and the contents of antioxidant substances, thereby maintaining the homeostasis of reactive oxygen species and reactive nitrogen species. Moreover, GSNOR also promoted photosynthesis in tobacco leaves at the transcriptional level. Through enrichment analysis of differentially expressed genes (DEGs) and weighted gene co-expression network analysis (WGCNA) based on physiological and RNA-seq data, it was found that photosynthesis-related pathways, including “Porphyrin and chlorophyll metabolism”, “Carbon fixation in photosynthetic organisms,” and “Photosynthesis,” were significantly enriched. In GSNOR-overexpression plants, the expression of genes encoding proteins involved in chlorophyll synthesis, the Calvin cycle, PSII, and PSI were upregulated. Meanwhile, leaf chlorophyll increased, and the net photosynthetic rate, stomatal conductance, and activity of the reaction centers were enhanced. In contrast, GSNOR-inhibited plants exhibited the opposite trends. These results indicate that NO enhances the salt tolerance of tobacco seedlings by promoting photosynthesis and enhancing antioxidant capacity.