The Fungal Effector Avr-Pita Suppresses Innate Immunity by Increasing COX Activity in Rice Mitochondria
文献类型： 外文期刊
作者： Han, Jingluan 1 ; Wang, Xiaoyu 1 ; Wang, Fengpin 1 ; Zhao, Zhe 1 ; Li, Gousi 1 ; Zhu, Xiaoyuan 4 ; Su, Jing 4 ; Chen, Let 1 ;
作者机构： 1.South China Agr Univ, State Key Lab Conservat & Utilizat Subtrop Agro B, Guangzhou 510642, Peoples R China
2.South China Agr Univ, Guangdong Prov Key Lab Prot Funct & Regulat Agr O, Guangzhou 510642, Peoples R China
3.South China Agr Univ, Coll Life Sci, Guangzhou 510642, Peoples R China
4.Guangdong Acad Agr Sci, Plant Protect Res Inst, Guangdong Prov Key Lab High Technol Plant Protect, Guangzhou 510640, Peoples R China
关键词： Innate immunity; Effector; Avr-Pita; Mitochondrion; Cytochrome c oxidase (COX); Reactive oxygen species (ROS)
期刊名称：RICE （ 影响因子：4.783； 五年影响因子：5.23 ）
ISSN： 1939-8425
年卷期： 2021 年 14 卷 1 期
页码：
收录情况： SCI
摘要： Background Avr-Pita was the first effector identified in the blast fungus (Magnaporthe oryzae)-rice (Oryza sativa) pathosystem. However, the molecular mechanism underlying its effects on the host plant has remained a long-standing mystery. Results Here, we report that ectopically expressing Avr-Pita in rice enhances susceptibility to M. oryzae and suppresses pathogen-associated molecular pattern (PAMP)-triggered defense responses. Avr-Pita targets the host mitochondria and interacts with the cytochrome c oxidase (COX) assembly protein OsCOX11, a key regulator of mitochondrial reactive oxygen species (ROS) metabolism in rice. Overexpressing Avr-Pita or OsCOX11 increased COX activity and decreased ROS accumulation triggered by the fungal PAMP chitin. OsCOX11-overexpressing plants showed increased susceptibility to M. oryzae, whereas OsCOX11-knockdown plants showed resistance to M. oryzae. Conclusions Taken together, these findings suggest that the fungal pathogen M. oryzae delivers the effector Avr-Pita to the host plant, where it enhances COX activity thus decreasing ROS accumulation. Therefore, this effector suppresses host innate immunity by perturbing ROS metabolism in the mitochondria.
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