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

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-Pi...

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Detalles Bibliográficos
Autores principales: Han, Jingluan, Wang, Xiaoyu, Wang, Fengpin, Zhao, Zhe, Li, Gousi, Zhu, Xiaoyuan, Su, Jing, Chen, Letian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7809080/
https://www.ncbi.nlm.nih.gov/pubmed/33443630
http://dx.doi.org/10.1186/s12284-021-00453-4
Descripción
Sumario: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. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12284-021-00453-4.