Scholarlink

Background <p>Salt stress is considered to be one of the major abiotic stresses influencing rice growth and productivity. To improve rice crop productivity in saline soils, it is essential to choose a suitable variety for mitigating salt stress and gain a deep understanding of the underlying mechanisms. The current study explored the salt tolerance mechanism of wild rice ‘<i>HD96-1</i> (salt resistive)’ and conventional rice ‘<i>IR29</i> (salt sensitive)’ by evaluating morph-physiological, transcriptomic, and metabolomic approaches.</p> Results <p>Physiological data indicated that <i>HD96-1</i> had higher chlorophyll content, higher photosynthetic efficiency, more stable Na<sup>+</sup>/K<sup>+</sup>, less H₂O₂, and lower electrolyte leakage under salt stress compared with <i>IR29</i>. Transcriptomic and metabolomic data showed that the expression of <i>NHXs</i> in <i>IR29</i> was significantly down-regulated under salt stress, leading to a large accumulation of Na⁺ in the cytoplasm, and that the expression of <i>CHLH</i>, <i>PORA</i>, and <i>PORB</i> was significantly down-regulated, inhibiting chlorophyll synthesis. <i>HD96-1</i> maintained the balance of Na⁺ and K⁺ by increasing the expression of <i>NHX4</i>, and there was no significant change in the expression of genes related to chlorophyll synthesis, which made <i>HD96-1</i> more resistant to salt stress than <i>IR29</i>. In addition, <i>HD96-1</i> inhibited the excessive synthesis of hydrogen peroxide (H₂O₂) and alleviated oxidative damage by significantly down-regulating the expression of <i>ACX4</i> under salt stress. <i>HD96-1</i> promoted the accumulation of isoleucine by up-regulating genes of branched-chain amino acid aminotransferase 2 and branched-chain amino acid aminotransferase 4 and might promote the synthesis of raffinose and stachyose by up-regulating the expression of the gene for galactitol synthase 2, which, in turn, maintained a stable osmotic pressure and relieved osmotic stress. We also found that <i>IR29</i> and <i>HD96-1</i> alleviated the inhibition of photosynthesis by salt stress by down-regulating the expression of light-harvesting chromophore protein complex (LHCH II)-related genes and reducing the excessive accumulation of glucose metabolites, respectively. In addition, <i>HD96-1</i> enhances salt tolerance by regulating <i>C2H2</i> and <i>bHLH153</i> transcription factors.</p> Conclusion <p>Under salt stress, <i>HD96-1</i> maintained ionic balance and photosynthetic efficiency by up-regulating the expression of <i>NHX4</i> gene and reducing the overaccumulation of glucose metabolites, respectively, and mitigated osmotic stress and oxidative stress by down-regulating the expression of <i>ACX4</i> and promoting the accumulation of isoleucine, respectively, thereby enhancing the adaptability to salt stress. <i>IR29</i> maintained photosynthetic efficiency under salt stress by down-regulating the expression of light-harvesting chromophore protein complex (LHCH II)-related genes, thereby enhancing adaptation to salt stress.</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

Integrative analysis of transcriptome and metabolome reveal molecular mechanism of tolerance to salt stress in rice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年3月15日

查看全文
  • Rui Deng,
  • Yao Li,
  • Nai-Jie Feng,
  • Dian-Feng Zheng,
  • Aaqil Khan,
  • You-Wei Du,
  • Jian-Qin Zhang,
  • Zhi-Yuan Sun,
  • Jia-Shuang Wu,
  • Ying-Bin Xue,
  • Zi-Hui Huang

摘要

Background

Salt stress is considered to be one of the major abiotic stresses influencing rice growth and productivity. To improve rice crop productivity in saline soils, it is essential to choose a suitable variety for mitigating salt stress and gain a deep understanding of the underlying mechanisms. The current study explored the salt tolerance mechanism of wild rice ‘HD96-1 (salt resistive)’ and conventional rice ‘IR29 (salt sensitive)’ by evaluating morph-physiological, transcriptomic, and metabolomic approaches.

Results

Physiological data indicated that HD96-1 had higher chlorophyll content, higher photosynthetic efficiency, more stable Na+/K+, less H₂O₂, and lower electrolyte leakage under salt stress compared with IR29. Transcriptomic and metabolomic data showed that the expression of NHXs in IR29 was significantly down-regulated under salt stress, leading to a large accumulation of Na⁺ in the cytoplasm, and that the expression of CHLH, PORA, and PORB was significantly down-regulated, inhibiting chlorophyll synthesis. HD96-1 maintained the balance of Na⁺ and K⁺ by increasing the expression of NHX4, and there was no significant change in the expression of genes related to chlorophyll synthesis, which made HD96-1 more resistant to salt stress than IR29. In addition, HD96-1 inhibited the excessive synthesis of hydrogen peroxide (H₂O₂) and alleviated oxidative damage by significantly down-regulating the expression of ACX4 under salt stress. HD96-1 promoted the accumulation of isoleucine by up-regulating genes of branched-chain amino acid aminotransferase 2 and branched-chain amino acid aminotransferase 4 and might promote the synthesis of raffinose and stachyose by up-regulating the expression of the gene for galactitol synthase 2, which, in turn, maintained a stable osmotic pressure and relieved osmotic stress. We also found that IR29 and HD96-1 alleviated the inhibition of photosynthesis by salt stress by down-regulating the expression of light-harvesting chromophore protein complex (LHCH II)-related genes and reducing the excessive accumulation of glucose metabolites, respectively. In addition, HD96-1 enhances salt tolerance by regulating C2H2 and bHLH153 transcription factors.

Conclusion

Under salt stress, HD96-1 maintained ionic balance and photosynthetic efficiency by up-regulating the expression of NHX4 gene and reducing the overaccumulation of glucose metabolites, respectively, and mitigated osmotic stress and oxidative stress by down-regulating the expression of ACX4 and promoting the accumulation of isoleucine, respectively, thereby enhancing the adaptability to salt stress. IR29 maintained photosynthetic efficiency under salt stress by down-regulating the expression of light-harvesting chromophore protein complex (LHCH II)-related genes, thereby enhancing adaptation to salt stress.