<p><i>OsTMS5</i> encodes a tRNA cyclic phosphatase, and its mutation causes male sterility under restrictive temperatures. However, the impact of the mutation of <i>OsTMS5</i> on the adaptability of rice to abiotic stress is poorly understood. Soil salinization is a major constraint for global rice production. Here, we demonstrate that a CRISPR/Cas9-mediated knockout of <i>OsTMS5</i> reduces salt tolerance in rice by disrupting reactive oxygen species (ROS) homeostasis. Under salt stress, <i>OsTMS5</i> knockout lines accumulated higher levels of H<sub>2</sub>O<sub>2</sub> and O<sub>2</sub><sup>−</sup>, and exhibited reduced activities of antioxidant enzymes including CAT and POD. In the root transcriptome, key differentially expressed genes were upregulated, including those involved in ROS production (<i>OsRboh</i>), scavenging (<i>OsPRX</i>) and signaling (MPK/SAPK kinases). Taken together, these results indicate that the salt sensitivity in <i>OsTMS5</i> knockout lines is caused by the dysregulated <i>OsRboh</i>-dependent ROS signaling, which is essential for activating stress-responsive genes in rice. Our findings provide a novel function of <i>OsTMS5</i> in salt tolerance and important information for the genetic improvement of salt-tolerant rice varieties.</p>

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OsTMS5 positively regulates salt tolerance by modulating reactive oxygen species homeostasis in rice (Oryza sativa L.)

  • Yue Hu,
  • Ruihao Wang,
  • Gengwei Wu,
  • Lanlan Wang,
  • Chi Zhang,
  • Xiaofang Zhu,
  • Xue Gong,
  • Dawei Xue,
  • Hua Wang

摘要

OsTMS5 encodes a tRNA cyclic phosphatase, and its mutation causes male sterility under restrictive temperatures. However, the impact of the mutation of OsTMS5 on the adaptability of rice to abiotic stress is poorly understood. Soil salinization is a major constraint for global rice production. Here, we demonstrate that a CRISPR/Cas9-mediated knockout of OsTMS5 reduces salt tolerance in rice by disrupting reactive oxygen species (ROS) homeostasis. Under salt stress, OsTMS5 knockout lines accumulated higher levels of H2O2 and O2, and exhibited reduced activities of antioxidant enzymes including CAT and POD. In the root transcriptome, key differentially expressed genes were upregulated, including those involved in ROS production (OsRboh), scavenging (OsPRX) and signaling (MPK/SAPK kinases). Taken together, these results indicate that the salt sensitivity in OsTMS5 knockout lines is caused by the dysregulated OsRboh-dependent ROS signaling, which is essential for activating stress-responsive genes in rice. Our findings provide a novel function of OsTMS5 in salt tolerance and important information for the genetic improvement of salt-tolerant rice varieties.