<p>Soil salinity severely inhibits rice growth. While the SBP-box gene <i>OsSPL10</i> is known to negatively regulate salt tolerance, its mechanism remains unclear. Since jasmonate (JA) mediates plant stress responses, we investigated the link between <i>OsSPL10</i> and JA in rice salt tolerance. Disrupting <i>OsSPL10</i> reduced the shoot Na<sup>+</sup>/K<sup>+</sup> ratio under salt stress, likely explaining the enhanced tolerance in <i>Osspl10</i> mutants. As leaves are highly sensitive to Na<sup>+</sup> toxicity, maintaining a low Na<sup>+</sup>/K<sup>+</sup> ratio is critical for survival. Notably, ten <i>OsJAZ</i> genes (JA repressors) were upregulated in <i>Osspl10</i> mutants. We found that <i>OsSPL10</i> directly suppresses certain <i>OsJAZ</i> genes (including <i>OsJAZ9</i>, known to regulate certain ion transporters), by binding to their promoters. These findings suggest that <i>OsSPL10</i> negatively modulate salt tolerance via the <i>OsJAZ</i>-mediated JA pathway, maintaining ion homeostasis. This study reveals new molecular mechanisms of rice salinity response, emphasizing the interplay between transcription factors and hormonal signaling.</p>

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OsSPL10 negatively regulates seedling salt tolerance through OsJAZ-mediated jasmonate pathway in rice (Oryza sativa L.)

  • Jilin Chen,
  • Tong Lan,
  • Tongtong Dong,
  • Qiaoling Liao,
  • Xiaoxiao An,
  • Chao Fang,
  • Xiaoxia Yang,
  • Xinle Cheng,
  • Kai Fan,
  • Xiaofang Xie,
  • Haitao Cui,
  • Weiren Wu,
  • Tao Lan

摘要

Soil salinity severely inhibits rice growth. While the SBP-box gene OsSPL10 is known to negatively regulate salt tolerance, its mechanism remains unclear. Since jasmonate (JA) mediates plant stress responses, we investigated the link between OsSPL10 and JA in rice salt tolerance. Disrupting OsSPL10 reduced the shoot Na+/K+ ratio under salt stress, likely explaining the enhanced tolerance in Osspl10 mutants. As leaves are highly sensitive to Na+ toxicity, maintaining a low Na+/K+ ratio is critical for survival. Notably, ten OsJAZ genes (JA repressors) were upregulated in Osspl10 mutants. We found that OsSPL10 directly suppresses certain OsJAZ genes (including OsJAZ9, known to regulate certain ion transporters), by binding to their promoters. These findings suggest that OsSPL10 negatively modulate salt tolerance via the OsJAZ-mediated JA pathway, maintaining ion homeostasis. This study reveals new molecular mechanisms of rice salinity response, emphasizing the interplay between transcription factors and hormonal signaling.