Ferroptosis in plant immunity.

Abstract

Plant cell death is mediated by calcium, iron, and reactive oxygen species (ROS) signaling in plant immunity. The reconstruction of a nucleotide-binding leucine-rich repeat receptor (NLR) supramolecular structure, called the resistosome, is intimately involved in the hypersensitive response (HR), a type of cell death involved in effector-triggered immunity (ETI). Iron is a crucial redox catalyst in various cellular reactions. Ferroptosis is a regulated, non-apoptotic form of iron- and ROS-dependent cell death in plants. Pathogen infections trigger iron accumulation and ROS bursts in plant cells, leading to lipid peroxidation via the Fenton reaction and subsequent ferroptosis in plant cells similar to that in mammalian cells. The small-molecule inducer erastin triggers iron-dependent lipid ROS accumulation and glutathione depletion, leading to HR cell death in plant immunity. Calcium (Ca²⁺) is another major mediator of plant immunity. Cytoplasmic Ca²⁺ influx through calcium-permeable channels, the resistosomes, mediates iron- and ROS-dependent ferroptotic cell death under reduced glutathione reductase (GR) expression levels in the ETI response in plants. Acibenzolar-S-methyl (ASM), a plant defense activator, enhances Ca²⁺ influx, ROS and iron accumulation and lipid peroxidation to trigger ferroptotic cell death in plants. These breakthroughs suggest a potential role of Ca²⁺ signaling in ferroptosis and its coordination with iron and ROS signaling in plant immunity. In this review, we highlight the essential roles of calcium, iron, and ROS signaling in ferroptosis during plant immunity and discuss advances in the understanding of how Ca²⁺-mediated ferroptotic cell death orchestrates effective plant immune responses against invading pathogens.