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<p>Rice kernel smut (RKS), caused by the basidiomycete fungus <i>Tilletia horrida</i>, is a major disease impacting the production of male sterile lines of rice (<i>Oryza sativa</i>) at the globally. Despite its significance, the understanding of mechanisms underlying resistance to RKS remain limited. This study employed map-based cloning to isolate the CC-NBS-LRR (CNL) RKS resistance gene OsnTNB.11 from the resistant rice line Jiangcheng3B. The knockout of OsnTNB.11 in Jiangcheng3B resulted in plants significantly more susceptible to <i>T. horrida</i> than the wild type. Stable OsnTNB.11 overexpression transgenic rice plants developed resistance against <i>T. horrida</i>. We further found that the coiled-coil (CC) domain of OsnTNB.11 (OsnTNB.11-CC) interacted with and stabilised rice methionine synthetases OsMETS1, a key enzyme involved in ethylene (ET) biosynthesis. OsnTNB.11 activated the transcriptional levels of ET-related defence genes and enhance ET contents, whereas the exogenous application of ACC (an ethylene biosynthesis precursor) improved rice resistance to <i>T. horrida</i>. Further, the introduction of OsnTNB.11 into a disease-susceptible rice variety promoted resistance to RKS without impacting grain yield. In summary, we determined a regulatory model of a novel RKS resistance mediated via the ET signalling pathway. These results enhance our understanding of RKS resistance mechanisms and provide a valuable genetic resource for resistant <i>T. horrida</i> rice male sterile lines for breeding.</p>

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OsnTNB.11 Encodes a CC-NBS-LRR Type Resistance Protein that Positively Regulates Resistance to Rice Kernel Smut by Modulating the Ethylene Signalling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月12日

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  • Xinyue Shu,
  • Desuo Yin,
  • Aiping Zheng,
  • Aijun Wang

摘要

Rice kernel smut (RKS), caused by the basidiomycete fungus Tilletia horrida, is a major disease impacting the production of male sterile lines of rice (Oryza sativa) at the globally. Despite its significance, the understanding of mechanisms underlying resistance to RKS remain limited. This study employed map-based cloning to isolate the CC-NBS-LRR (CNL) RKS resistance gene OsnTNB.11 from the resistant rice line Jiangcheng3B. The knockout of OsnTNB.11 in Jiangcheng3B resulted in plants significantly more susceptible to T. horrida than the wild type. Stable OsnTNB.11 overexpression transgenic rice plants developed resistance against T. horrida. We further found that the coiled-coil (CC) domain of OsnTNB.11 (OsnTNB.11-CC) interacted with and stabilised rice methionine synthetases OsMETS1, a key enzyme involved in ethylene (ET) biosynthesis. OsnTNB.11 activated the transcriptional levels of ET-related defence genes and enhance ET contents, whereas the exogenous application of ACC (an ethylene biosynthesis precursor) improved rice resistance to T. horrida. Further, the introduction of OsnTNB.11 into a disease-susceptible rice variety promoted resistance to RKS without impacting grain yield. In summary, we determined a regulatory model of a novel RKS resistance mediated via the ET signalling pathway. These results enhance our understanding of RKS resistance mechanisms and provide a valuable genetic resource for resistant T. horrida rice male sterile lines for breeding.