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转录组和代谢组的综合分析揭示了水稻耐盐胁迫的分子机制。

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

作者信息

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

机构信息

College of Coastal Agriculture Sciences, Guangdong Ocean University, Zhanjiang, 524088, China.

South China Center of National Saline-tolerant Rice Technology Innovation Center, Zhanjiang, 524088, China.

出版信息

BMC Plant Biol. 2025 Mar 15;25(1):335. doi: 10.1186/s12870-025-06300-8.

DOI:10.1186/s12870-025-06300-8
PMID:40089670
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11909974/
Abstract

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.

摘要

背景

盐胁迫被认为是影响水稻生长和生产力的主要非生物胁迫之一。为提高盐碱地水稻作物的生产力,选择合适的品种来减轻盐胁迫并深入了解其潜在机制至关重要。本研究通过评估形态生理、转录组和代谢组学方法,探索了野生稻“HD96 - 1(耐盐)”和常规稻“IR29(盐敏感)”的耐盐机制。

结果

生理数据表明,与IR29相比,HD96 - 1在盐胁迫下具有更高的叶绿素含量、更高的光合效率、更稳定的钠钾比、更少的过氧化氢和更低的电解质渗漏率。转录组和代谢组数据显示,盐胁迫下IR29中NHXs的表达显著下调,导致细胞质中Na⁺大量积累,并且CHLH、PORA和PORB的表达显著下调,抑制了叶绿素合成。HD96 - 1通过增加NHX4的表达维持了Na⁺和K⁺的平衡,与叶绿素合成相关的基因表达没有显著变化,这使得HD96 - 1比IR29更耐盐胁迫。此外,HD96 - 1在盐胁迫下通过显著下调ACX4的表达抑制了过氧化氢(H₂O₂)的过度合成并减轻了氧化损伤。HD96 - 1通过上调支链氨基酸转氨酶2和支链氨基酸转氨酶4的基因促进了异亮氨酸的积累,并且可能通过上调半乳糖醇合酶2基因的表达促进了棉子糖和水苏糖的合成,进而维持了稳定的渗透压并缓解了渗透胁迫。我们还发现,IR29和HD96 - 1分别通过下调捕光色素蛋白复合体(LHCH II)相关基因的表达和减少葡萄糖代谢物的过度积累,减轻了盐胁迫对光合作用的抑制。此外,HD96 - 1通过调节C2H2和bHLH153转录因子增强了耐盐性。

结论

在盐胁迫下,HD96 - 1分别通过上调NHX4基因的表达和减少葡萄糖代谢物的过度积累维持了离子平衡和光合效率,并分别通过下调ACX4的表达和促进异亮氨酸的积累减轻了渗透胁迫和氧化胁迫,从而增强了对盐胁迫的适应性。IR29通过下调捕光色素蛋白复合体(LHCH II)相关基因的表达在盐胁迫下维持了光合效率,从而增强了对盐胁迫的适应性。

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