Researchers highlight ferroptosis's dual roles in plant immunity

When plants encounter pathogens, they can defend themselves by rapidly killing infected cells to restrict pathogen spread. This immune response, known as the hypersensitive response (HR), was first described in 1915. However, the molecular mechanism underlying HR cell death remained poorly understood for more than a century.

In 2019, Professor Nam-Soo Jwa's research team at Sejong University made a pioneering discovery demonstrating that HR cell death in rice involves ferroptosis, an iron- and reactive oxygen species (ROS)-dependent form of regulated cell death. Published in The Plant Cell, this study provided a molecular explanation for how immune signaling leads to cell death and disease resistance.

Ferroptosis occurs when iron and ROS promote lipid peroxidation, ultimately causing cell death. Although extensively studied in animals, particularly in relation to cancer and neurodegenerative diseases, ferroptosis has emerged as an important mechanism in plant immunity.

Building on their original discovery, Jwa's team has continued to identify genetic regulators connecting immune signaling to ferroptotic cell death. Most recently, in February 2026, the team reported in Plant Communications that the rice phospholipase C4 gene (OsPLC4) amplifies calcium and ROS signaling to promote ferroptotic HR and disease resistance.

A newly published international collaborative study brings together researchers who pioneered the discovery of ferroptosis in both plants and fungal pathogens. The findings are published in the journal iMeta.

Professor Jwa, who first demonstrated ferroptosis in plant immunity in 2019, collaborated with Professor Naweed I. Naqvi of the National University of Singapore and Professor Yi-Zhen Deng of South China Agricultural University, whose research established ferroptosis in the rice blast fungus in 2020.

Remarkably, ferroptosis plays contrasting roles in these interacting organisms. In rice, it contributes to immune defense by eliminating infected cells, whereas in the rice blast fungus, it supports developmental processes required for successful infection.

By integrating multi-omics evidence, the researchers present a unified framework linking iron metabolism, ROS production, lipid peroxidation, calcium signaling and autophagy to explain these contrasting roles.

This study provides a broader framework for understanding how ferroptosis is executed and regulated during plant–pathogen interactions. It also opens new possibilities for improving crop disease resistance by selectively controlling ferroptosis in plants and their pathogens.

Professor Jwa emphasized that his ongoing research aims to determine whether ferroptosis represents a conserved mechanism of immune cell death across diverse plant species. Understanding how its timing and intensity are regulated may ultimately contribute to the development of disease-resistant crops and environmentally sustainable disease management strategies.