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Reference Detail
| Reference | ||
|---|---|---|
| Author | Nguyen N.K., Liu D., Wang J., Hwang B.K., Jwa N.S. | |
| Title | Rice phospholipase C4 enhances Ca2+ and ROS bursts during effector-triggered immunity to induce ferroptotic cell death. | |
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Abstract: Phospholipases are major regulators of lipid-dependent signaling and play crucial roles in plant immunity. Rice (Oryza sativa) phospholipase C4 (Osplc4) is a major functional enzyme in the rice phospholipase family that regulates intracellular Ca2+ levels. Here we show that Osplc4 translocates primarily to the plasma membrane in a Ca2+-dependent manner, with its C2 domain functioning as a membrane trafficker. Transient expression of Osplc4 and its truncated variants triggers cell death and immune responses in plants. During effector-triggered immunity (ETI) in rice, Osplc4 expression and Ca2+ influx are specifically and strongly induced in response to avirulent Magnaporthe oryzae. Upon infection, the rice Osplc4 knockout mutant (ΔOsplc4) exhibits substantially reduced Ca2+, reactive oxygen species (ROS), and Fe3+ accumulation, as well as diminished lipid peroxidation and hypersensitive response (HR) cell death. Complementation of ΔOsplc4 can fully restore Ca2+-mediated ferroptotic cell death. Osplc4 expression also activates HR cell death and the expression of defense-related genes such as OsRbohB, OsMEK2, OsMPK1, and OsPAL1 during avirulent M. oryzae infection. The Ca2+ chelator ethylene glycol-bis(2-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) substantially inhibits Ca2+, ROS, and Fe3+ accumulation and HR-related cell death in rice, whereas the Ca2+ influx enhancers trifluoperazine hydrochloride (TFP) and acibenzolar-S-methyl (ASM) strongly induce Ca2+-mediated ferroptotic cell death. Additionally, Osplc4 overexpression triggers cell death and immune responses in Arabidopsis. Collectively, our findings demonstrate that Osplc4 acts as a downstream target of resistosome activation and sustains the co-elevation of Ca2+ and ROS levels during rice ETI, thereby promoting Ca2+-mediated, lipid ROS-dependent ferroptotic cell death. These results establish Osplc4 as a key regulator of Ca2+-dependent plant immunity. |
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| Journal | Plant Commun | |
| Country | South Korea | |
| Volume | 7(1) | |
| Pages | 101589 | |
| Year | 2026 | |
| PubMed ID | 41220176 | |
| PubMed Central ID | 12902295 | |
| DOI | 10.1016/j.xplc.2025.101589 | |
| URL | - | |
| Relation | ||
| Gene | DSG1 MKK1 PLC4 RBOHB _ | |
| INSD | - | |
| Strain | Wild Core Collection | - |
| Induced Mutation Lines(NIG Collection) | - | |
| Sterile Seed Strain | - | |
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Lethal Embryo Mutantion Strain |
- | |
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Stages in Each Organ - Muant Lines (Gene) |
- | |
| Cultivated Varieties(NIG Collection) | - | |
| Stages in Each Organ | - | |
