Scholarlink

<p>Cross-kingdom RNA interference (RNAi) is a key virulence mechanism in which pathogens deliver small RNAs (sRNAs) into host plants, hijacking host ARGONAUTE (AGO) proteins to silence immunity-related genes. However, systematic studies on cross-kingdom RNAi in staple crops, such as rice, remain lacking. Moreover, the mechanism by which plants modulate cross-kingdom RNAi to restrict pathogen invasion is unknown. Here, we identify OsAGO proteins potentially hijacked by <i>R. solani</i> and perform comprehensive sRNA sequencing to profile fungal-derived sRNAs targeting rice genes. Our analysis reveals two <i>R. solani</i>-derived sRNAs that specifically bind OsAGO1 to silence two rice defense genes: <i>Cytochrome P450 98A1</i> (<i>OsCYP98A1</i>) and <i>NIMA-related kinase 6</i> (<i>OsNEK6</i>). Notably, we find that <i>OsmiR168</i> fine-tunes cross-kingdom RNAi efficiency by regulating <i>OsAGO1</i> mRNA levels. More importantly, a long non-coding RNA, <i>LncRNA19164</i>, acts as a competing endogenous RNA (ceRNA) to sequester <i>OsmiR168</i>, thereby stabilizing <i>OsAGO1</i> transcripts and regulating cross-kingdom RNAi. Our findings not only advance the understanding of cross-kingdom RNAi in plant-pathogen interactions but also provide a foundation for developing RNA-based disease control strategies in crops.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

A rice ceRNA module suppresses Rhizoctonia solani–induced cross-kingdom RNAi to reduce fungal pathogenicity

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月22日

查看全文
  • Jile Ni,
  • Wanpeng Mao,
  • Ting Shi,
  • Yeli Qin,
  • Wei Li,
  • Qiang Cai

摘要

Cross-kingdom RNA interference (RNAi) is a key virulence mechanism in which pathogens deliver small RNAs (sRNAs) into host plants, hijacking host ARGONAUTE (AGO) proteins to silence immunity-related genes. However, systematic studies on cross-kingdom RNAi in staple crops, such as rice, remain lacking. Moreover, the mechanism by which plants modulate cross-kingdom RNAi to restrict pathogen invasion is unknown. Here, we identify OsAGO proteins potentially hijacked by R. solani and perform comprehensive sRNA sequencing to profile fungal-derived sRNAs targeting rice genes. Our analysis reveals two R. solani-derived sRNAs that specifically bind OsAGO1 to silence two rice defense genes: Cytochrome P450 98A1 (OsCYP98A1) and NIMA-related kinase 6 (OsNEK6). Notably, we find that OsmiR168 fine-tunes cross-kingdom RNAi efficiency by regulating OsAGO1 mRNA levels. More importantly, a long non-coding RNA, LncRNA19164, acts as a competing endogenous RNA (ceRNA) to sequester OsmiR168, thereby stabilizing OsAGO1 transcripts and regulating cross-kingdom RNAi. Our findings not only advance the understanding of cross-kingdom RNAi in plant-pathogen interactions but also provide a foundation for developing RNA-based disease control strategies in crops.