Journal
PLANT CELL
Volume 31, Issue 1, Pages 189-209Publisher
OXFORD UNIV PRESS INC
DOI: 10.1105/tpc.18.00535
Keywords
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Funding
- Cooperative Research Program for Agriculture Science and Technology Development, Rural Development Administration, Republic of Korea [PJ013419]
- Basic Science Research Program through National Research Foundation of Korea - Ministry of Education [2016R1D1A1A09918756]
- National Research Foundation of Korea [2016R1D1A1A09918756] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Hypersensitive response (HR) cell death is the most effective plant immune response restricting fungal pathogen invasion. Here, we report that incompatible rice (Oryza sativa) Magnaporthe oryzae interactions induce iron-and reactive oxygen species (ROS)-dependent ferroptotic cell death in rice cells. Ferric ions and ROS (i. e., H2O2) accumulated in tissues undergoing HR cell death of rice leaf sheath tissues during avirulent M. oryzae infection. By contrast, iron did not accumulate in rice cells during virulent M. oryzae infection or treatment with the fungal elicitor chitin. Avirulent M. oryzae infection in DOsnadp- me2-3 mutant rice did not trigger iron and ROS accumulation and suppressed HR cell death, suggesting that NADPmalic enzyme2 is required for ferroptotic cell death in rice. The small-molecule ferroptosis inhibitors deferoxamine, ferrostatin-1, and cytochalasin E and the NADPH oxidase inhibitor diphenyleneiodonium suppressed iron-dependent ROS accumulation and lipid peroxidation to completely attenuate HR cell death in rice sheaths during avirulent M. oryzae infection. By contrast, the small-molecule inducer erastin triggered iron-dependent ROS accumulation and glutathione depletion, which ultimately led to HR cell death in rice in response to virulent M. oryzae. These combined results demonstrate that iron-and ROS-dependent signaling cascades are involved in the ferroptotic cell death pathway in rice to disrupt M. oryzae infection.
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