The Fungal Effector Avr-Pita Suppresses Innate Immunity by Increasing COX Activity in Rice Mitochondria

被引:58
作者
Han, Jingluan [1 ,2 ,3 ]
Wang, Xiaoyu [1 ,3 ]
Wang, Fengpin [1 ,3 ]
Zhao, Zhe [1 ,2 ,3 ]
Li, Gousi [1 ,3 ]
Zhu, Xiaoyuan [4 ]
Su, Jing [4 ]
Chen, Letian [1 ,2 ,3 ]
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
基金
中国国家自然科学基金;
关键词
Innate immunity; Effector; Avr-Pita; Mitochondrion; Cytochrome c oxidase (COX); Reactive oxygen species (ROS);
D O I
10.1186/s12284-021-00453-4
中图分类号
S3 [农学(农艺学)];
学科分类号
0901 ;
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.
引用
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页数:11
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