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Ca2+ sensor-mediated ROS scavenging suppresses rice immunity and is exploited by a fungal effector
Author(s) -
Mingjun Gao,
Yang He,
Xin Yin,
Xiangbin Zhong,
Bingxiao Yan,
Yue Wu,
Jin Chen,
Xiaoyuan Li,
Keran Zhai,
Yifeng Huang,
Xiangyu Gong,
Huizhong Chang,
Shenghan Xie,
Jiyun Liu,
JiaXing Yue,
Jianlong Xu,
Guiquan Zhang,
Yiwen Deng,
Ertao Wang,
Didier Tharreau,
GuoLiang Wang,
Weibing Yang,
Zuhua He
Publication year - 2021
Publication title -
cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 26.304
H-Index - 776
eISSN - 1097-4172
pISSN - 0092-8674
DOI - 10.1016/j.cell.2021.09.009
Subject(s) - biology , effector , plant immunity , immunity , reactive oxygen species , immune system , microbiology and biotechnology , pathogen , virulence , plant disease resistance , homeostasis , genetics , arabidopsis , mutant , gene
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 Ca 2+ -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 Ca 2+ sensing and ROS homeostasis to suppress plant immunity, suggesting a principle for breeding disease-resistant, high-yield crops.

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