The <scp>O</scp>s<scp>FBX</scp>388‐<scp>O</scp>s<scp>FIP</scp>1‐<scp>O</scp>s<scp>C</scp>at<scp>A</scp> module regulates <scp>ROS</scp> homeostasis and disease resistance in rice

Plants are exposed to various biotic and abiotic environmental stresses, resulting in the generation of reactive oxygen species (ROS). One of the enzymes responsible for neutralizing excess ROS is catalase (CAT), which breaks down hydrogen peroxide (H₂O₂). However, the regulation of CAT in mediating H₂O₂ homeostasis remains unclear. Here, we report that the DUF1644-containing protein OsFIP1 modulates H₂O₂ homeostasis and positively regulates rice immunity. Overexpression (OE) of OsFIP1 leads to enhanced resistance against rice blast disease, accompanied by upregulation of defense-related genes, enhanced chitin-induced ROS burst and H₂O₂ accumulation. Furthermore, OsFIP1 interacts with OsCatA. OE of OsFIP1 dramatically reduces accumulation of OsCatA in cytoplasm. Presence of OsFIP1 reduces OsCatA's tetramerization and CAT activity. Consistently, the knockout (KN) of OsCatA leads to enhanced resistance to rice blast. The E3 ligase OsFBX388 interacts with and ubiquitinates OsFIP1 for degradation. KN of OsFBX388 leads to overaccumulation of OsFIP1 and reduced CAT activity, thereby resulting in enhanced ROS burst and blast resistance. These findings highlight the crucial role of the OsFBX388-OsFIP1-OsCatA module in mediating ROS homeostasis and disease resistance, offering new insights into the mechanisms underlying immunity.