A pathogen lncRNA secreted into rice sequesters a host miRNA for virulence
6 affiliations
- 1New Cornerstone Science Laboratory, State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Rice Research Institute, Sichuan Agricultural University, Chengdu, China. [email protected]
- 2New Cornerstone Science Laboratory, State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Rice Research Institute, Sichuan Agricultural University, Chengdu, China
- 3Education Ministry Key Laboratory of Medical Electrophysiology, Sichuan Key Medical Laboratory of New Drug Discovery and Druggability Evaluation, School of Pharmacy, Southwest Medical University, Luzhou, China
- 4Forest Ecology and Conservation in the Upper Reaches of the Yangtze River Key Laboratory of Sichuan Province, Mianyang Teachers' College, Mianyang, China
- 5Department of Plant Pathology, University of California, Davis, Davis, CA, USA
- 6New Cornerstone Science Laboratory, State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Rice Research Institute, Sichuan Agricultural University, Chengdu, China. [email protected]
Abstract
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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BibTeX
@article{he2026pathogen,
title = {{A pathogen lncRNA secreted into rice sequesters a host miRNA for virulence}},
author = {Min He and Jia Su and Xiaogang Zhou and Tuo Qi and Jiazheng Wang and Tianxin Zhang and Jinhua Chen and Mawsheng Chern and Youpin Xu and Xiang Lu and Qingqing Hou and Hongrui Liu and Wenfang Huang and Jiawei Liu and Shiying Li and Yunfei Zhu and Xue Chen and Senyu Ran and Han Li and Renju Liu and Mingliang Lei and Guosong Shu and Haicheng Liao and Junjie Yin and Xiang Lu and Yongyan Tang and Li Song and Long Wang and Qing Ping Xiong and Jiali Liu and Yu Bi and Yihua Yang and Hai Qing and 马炳田 and Yan Li and Jing Fan and Peng Qin and Yuping Wang and Jianming Wu and Wenming Wang and Shigui Li and Weitao Li and Jing Wang and Xuewei Chen},
journal = {Nature},
year = {2026},
month = may,
doi = {10.1038/s41586-026-10572-x},
url = {https://doi.org/10.1038/s41586-026-10572-x},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - A pathogen lncRNA secreted into rice sequesters a host miRNA for virulence
AU - Min He
AU - Jia Su
AU - Xiaogang Zhou
AU - Tuo Qi
AU - Jiazheng Wang
AU - Tianxin Zhang
AU - Jinhua Chen
AU - Mawsheng Chern
AU - Youpin Xu
AU - Xiang Lu
AU - Qingqing Hou
AU - Hongrui Liu
AU - Wenfang Huang
AU - Jiawei Liu
AU - Shiying Li
AU - Yunfei Zhu
AU - Xue Chen
AU - Senyu Ran
AU - Han Li
AU - Renju Liu
AU - Mingliang Lei
AU - Guosong Shu
AU - Haicheng Liao
AU - Junjie Yin
AU - Xiang Lu
AU - Yongyan Tang
AU - Li Song
AU - Long Wang
AU - Qing Ping Xiong
AU - Jiali Liu
AU - Yu Bi
AU - Yihua Yang
AU - Hai Qing
AU - 马炳田
AU - Yan Li
AU - Jing Fan
AU - Peng Qin
AU - Yuping Wang
AU - Jianming Wu
AU - Wenming Wang
AU - Shigui Li
AU - Weitao Li
AU - Jing Wang
AU - Xuewei Chen
PY - 2026
DA - 2026/05/20
JO - Nature
DO - 10.1038/s41586-026-10572-x
UR - https://doi.org/10.1038/s41586-026-10572-x
AB - 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.
SN - 0028-0836
SN - 1476-4687
ER -