| Literature DB >> 34597584 |
Mingjun Gao1, Yang He1, Xin Yin2, Xiangbin Zhong3, Bingxiao Yan1, Yue Wu1, Jin Chen1, Xiaoyuan Li4, Keran Zhai1, Yifeng Huang1, Xiangyu Gong1, Huizhong Chang1, Shenghan Xie4, Jiyun Liu1, Jiaxing Yue5, Jianlong Xu6, Guiquan Zhang7, Yiwen Deng1, Ertao Wang1, Didier Tharreau8, Guo-Liang Wang9, Weibing Yang10, Zuhua He11.
Abstract
Plant immunity is activated upon pathogen perception and often affects growth and yield when it is constitutively active. How plants fine-tune immune homeostasis in their natural habitats remains elusive. Here, we discover a conserved immune suppression network in cereals that orchestrates immune homeostasis, centering on a Ca2+-sensor, RESISTANCE OF RICE TO DISEASES1 (ROD1). ROD1 promotes reactive oxygen species (ROS) scavenging by stimulating catalase activity, and its protein stability is regulated by ubiquitination. ROD1 disruption confers resistance to multiple pathogens, whereas a natural ROD1 allele prevalent in indica rice with agroecology-specific distribution enhances resistance without yield penalty. The fungal effector AvrPiz-t structurally mimics ROD1 and activates the same ROS-scavenging cascade to suppress host immunity and promote virulence. We thus reveal a molecular framework adopted by both host and pathogen that integrates Ca2+ sensing and ROS homeostasis to suppress plant immunity, suggesting a principle for breeding disease-resistant, high-yield crops.Entities:
Keywords: Ca(2+)-sensor; E3 ubiquitin ligases; ROD1; catalase; disease resistance; fungal effector; natural variation; reactive oxygen species; rice immunity; structural mimicry
Mesh：
Substances：
Year: 2021 PMID： 34597584 DOI： 10.1016/j.cell.2021.09.009
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 66.850