生物
效应器
小RNA
基因
核糖核酸
遗传学
DNA
病菌
毒力
寄主(生物学)
基因沉默
基因表达调控
RNA沉默
基因表达
细胞生物学
RNA干扰
基因组
免疫
小干扰RNA
外源DNA
麦格纳波特
DNA测序
小RNA
信使核糖核酸
调节器
阿尔戈瑙特
基因组DNA
DNA损伤
调节顺序
宿主-病原体相互作用
作者
Min He,Jia Su,Xiaogang Zhou,Tuo Qi,Yì Wáng,Tianxin Zhang,Jinhua Chen,Mawsheng Chern,Youpin Xu,Xiang Lu,Qingqing Hou,Hongrui Liu,Wenfang Huang,Jiawei Liu,Shiying Li,Yunfei Zhu,Xue Chen,Senyu Ran,Hui Li,Renju Liu
出处
期刊:Nature
[Nature Portfolio]
日期:2026-05-20
标识
DOI:10.1038/s41586-026-10572-x
摘要
Plants and animals respond to pathogens through pattern recognition receptor and Nod-like receptor proteins1. Pathogens commonly use protein effectors to suppress host immunity for successful infection2. However, the existence of non-protein effector classes remains comparatively understudied. Here we report an RNA–RNA recognition mechanism governing pathogen–host interaction, mediated by a regulatory RNA-encoding DNA sequence that separately generates two complementary regulatory RNAs. Specifically, a long non-coding RNA transcribed from this DNA region in the fungal pathogen Magnaporthe oryzae translocates into host rice cells and sequesters a complementary microRNA (miRNA), derived from a distinct host DNA region, thereby subverting host immunity. In turn, this rice-derived miRNA promotes disease resistance by repressing the expression of PKR1, a gene that encodes a negative regulator of host immunity. Sequestration of the host miRNA by the fungal long non-coding RNA releases PKR1 expression to facilitate fungal infection. We discovered that this regulatory RNA-encoding DNA sequence is probably widely present across diverse life species, mediating interactions between pathogens and their plant hosts. Collectively, our findings provide an approach for effective disease control using miRNAs derived from this important DNA region. A fungal long non-coding RNA from Magnaporthe oryzae translocates into rice cells to sequester a host microRNA that normally represses PKR1, a negative immunity regulator, thereby facilitating infection and revealing a widespread RNA-based pathogen–host interaction mechanism.
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