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Published on: March 15, 2024
Rice phospholipase C4 enhances Ca2+ and ROS bursts during effector-triggered immunity to induce ferroptotic cell
Nam Khoa Nguyen1, Dongping Liu1, Juan Wang1
1Division of Integrative Bioscience and Biotechnology, College of Life Sciences, Sejong University, Seoul 05006, Republic of Korea.
Rice phospholipase C4 (OsPLC4) regulates plant immunity by controlling calcium (Ca2+) levels. OsPLC4 is crucial for effector-triggered immunity (ETI), promoting cell death and defense responses against pathogens.
Area of Science:
- Plant Biology
- Molecular Plant Pathology
- Plant Biochemistry
Background:
- Phospholipases are key regulators of lipid signaling and plant immunity.
- Rice phospholipase C4 (OsPLC4) influences intracellular calcium (Ca2+) levels.
Purpose of the Study:
- To investigate the role of OsPLC4 in rice immunity and calcium signaling.
- To elucidate the mechanism of OsPLC4-mediated cell death and defense responses.
Main Methods:
- Transient expression of OsPLC4 and variants in plants.
- Analysis of Osplc4 knockout mutants during Magnaporthe oryzae infection.
- Biochemical assays for Ca2+, reactive oxygen species (ROS), and Fe3+ accumulation.
- Treatment with Ca2+ chelators and enhancers.
- OsPLC4 overexpression in Arabidopsis.
Main Results:
- OsPLC4 translocates to the plasma membrane in a Ca2+-dependent manner.
- OsPLC4 triggers cell death and immune responses.
- Osplc4 knockout mutants show reduced Ca2+, ROS, Fe3+ accumulation, and cell death.
- OsPLC4 promotes Ca2+-mediated ferroptotic cell death and activates defense genes.
- OsPLC4 overexpression induces immunity in Arabidopsis.
Conclusions:
- OsPLC4 is a critical regulator of Ca2+-dependent plant immunity.
- OsPLC4 acts downstream of resistosome activation, sustaining Ca2+ and ROS elevation during ETI.
- OsPLC4 promotes lipid ROS-dependent ferroptotic cell death, enhancing plant defense.
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