Iron- and reactive oxygen species (ROS)-dependent ferroptosis occurs in plant cells. Ca2+acts as a conserved key mediator to control plant immune responses. Here, we report a novel role of cytoplasmic Ca2+influx regulating ferroptotic cell death in rice immunity using pharmacological approaches. High Ca2+influx triggered iron-dependent ROS accumulation, lipid peroxidation, and subsequent hypersensitive response (HR) cell death in rice (Oryza sativa). DuringMagnaporthe oryzaeinfection, 14 different Ca2+influx regulators altered Ca2+, ROS and Fe2+accumulation,glutathione reductase(GR) expression, glutathione (GSH) depletion and lipid peroxidation, leading to ferroptotic cell death in rice. High Ca2+levels inhibited the reduction of glutathione isulphide (GSSG) to GSHin vitro. Ca2+chelation by ethylene glycol-bis (2-aminoethylether)-N, N, N’, N’-tetra-acetic acid (EGTA) suppressed apoplastic Ca2+influx in rice leaf sheaths during infection. Blocking apoplastic Ca2+influx into the cytoplasm by Ca2+chelation effectively suppressed Ca2+-mediated iron-dependent ROS accumulation and ferroptotic cell death. By contrast, acibenzolar-S-methyl (ASM), a plant defense activator, significantly enhanced Ca2+influx, as well as ROS and iron accumulation to trigger ferroptotic cell death in rice. The cytoplasmic Ca2+influx through calcium-permeable cation channels, including the putative resistosomes, could mediate iron- and ROS-dependent ferroptotic cell death under reducedGRexpression levels in rice immune responses.
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Plant “helper” immune receptors are Ca 2+ -permeable nonselective cation channels
Plant nucleotide-binding leucine-rich repeat receptors (NLRs) regulate immunity and cell death. InArabidopsis, a subfamily of “helper” NLRs is required by many “sensor” NLRs. Active NRG1.1 oligomerized, was enriched in plasma membrane puncta, and conferred cytoplasmic calcium ion (Ca2+) influx in plant and human cells. NRG1.1-dependent Ca2+influx and cell death were sensitive to Ca2+channel blockers and were suppressed by mutations affecting oligomerization or plasma membrane enrichment. Ca2+influx and cell death mediated by NRG1.1 and ACTIVATED DISEASE RESISTANCE 1 (ADR1), another helper NLR, required conserved negatively charged N-terminal residues. Whole-cell voltage-clamp recordings demonstrated thatArabidopsishelper NLRs form Ca2+-permeable cation channels to directly regulate cytoplasmic Ca2+levels and consequent cell death. Thus, helper NLRs transduce cell death signals directly.
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- Award ID(s):
- 1758400
- PAR ID:
- 10279138
- Publisher / Repository:
- American Association for the Advancement of Science (AAAS)
- Date Published:
- Journal Name:
- Science
- Volume:
- 373
- Issue:
- 6553
- ISSN:
- 0036-8075
- Page Range / eLocation ID:
- p. 420-425
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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