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<p>Salinity stress constitutes a primary environmental constraint that severely limits rice productivity. In this study, we identified the B-type response regulator <i>OsRR41</i> as an indispensable positive regulator of salinity tolerance in rice. Utilizing CRISPR/Cas9 technology, we generated knockout the three independent mutant lines, which exhibited hypersensitivity to salt stress. Under salt stress conditions, these mutants displayed more pronounced growth retardation compared to wild-type plants, characterized by significantly reduced biomass, severe leaf chlorosis, and accelerated wilting. Physiologically, the loss of <i>OsRR41</i> resulted in an inability to maintain cellular homeostasis, leading to excessive accumulation of reactive oxygen species (ROS) causing oxidative damage, and a severely disrupted ionic balance manifested by elevated Na<sup>+</sup>/K<sup>+</sup> ratios. Combined transcriptomic and metabolomic analyses indicated that the loss of <i>OsRR41</i> function leads to widespread disruption of stress-responsive gene expression networks and metabolic homeostasis. Our findings thus establish <i>OsRR41</i> as a pivotal regulatory node conferring salinity tolerance in rice by orchestrating essential physiological and metabolic defense responses under stress conditions.</p>

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Genome-wide identification of the ARR-B gene family and functional characterization of OsRR41 as a positive regulator of salinity tolerance in rice

  • 期刊论文

  • 发表日期：

    2026年4月9日

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  • Huashuai Cao,
  • Shilin Ding,
  • Kunjie Li,
  • Longhui Zhang,
  • Yuting Yi,
  • Chenyang Li,
  • Yingxin Qiu,
  • Lvni Tan,
  • Quanqiang Lei,
  • Weijun Chen,
  • Bin Li,
  • Yixing Li,
  • Shufeng Song,
  • Yi Pan,
  • Li Li

摘要

Salinity stress constitutes a primary environmental constraint that severely limits rice productivity. In this study, we identified the B-type response regulator OsRR41 as an indispensable positive regulator of salinity tolerance in rice. Utilizing CRISPR/Cas9 technology, we generated knockout the three independent mutant lines, which exhibited hypersensitivity to salt stress. Under salt stress conditions, these mutants displayed more pronounced growth retardation compared to wild-type plants, characterized by significantly reduced biomass, severe leaf chlorosis, and accelerated wilting. Physiologically, the loss of OsRR41 resulted in an inability to maintain cellular homeostasis, leading to excessive accumulation of reactive oxygen species (ROS) causing oxidative damage, and a severely disrupted ionic balance manifested by elevated Na+/K+ ratios. Combined transcriptomic and metabolomic analyses indicated that the loss of OsRR41 function leads to widespread disruption of stress-responsive gene expression networks and metabolic homeostasis. Our findings thus establish OsRR41 as a pivotal regulatory node conferring salinity tolerance in rice by orchestrating essential physiological and metabolic defense responses under stress conditions.