A non-canonical DWARF3-OsCOX11-mediated mitochondrial ROS homeostasis pathway acts in parallel with core strigolactone signaling to promote rice blast resistance.

Strigolactones (SLs) are a class of plant hormones with multifaceted roles in rice (Oryza sativa L.) growth and development. The F-box protein DWARF3 (D3) is a core component of the SL signalling pathway, coupling SL perception to the downstream responses. However, whether D3 also contributes to rice immunity and how it functions in this process remain unclear. Here, we analysed D3 allelic mutants carrying deletions in F-box- or C-terminal helix (CTH) domains. These mutants exhibited increased susceptibility to Magnaporthe oryzae, and differentially affected the expression of PHENYLALANINE AMMONIA LYASE genes and lignin accumulation, indicating that this canonical SL-regulated pathway contributes to, but does not fully account for, D3-mediated blast resistance. Yeast two-hybrid screening identified OsCOX11, a cytochrome c oxidase (COX) assembly factor, as a D3-interacting protein. D3 promotes the ubiquitination and degradation of OsCOX11, thereby modulating mitochondrial function and reactive oxygen species (ROS) accumulation during immune responses. Loss of D3 function resulted in increased COX activity, aberrant mitochondrial morphology, and compromised elicitor-induced ROS burst, particularly in the CTH-truncated line. Notably, rac-GR24 activated canonical SL signalling but did not measurably alter the D3-OsCOX11 interaction, OsCOX11 abundance, or COX activity under the tested conditions. Together, our findings identify a D3-OsCOX11 mitochondrial branch that operates in parallel with core D3-DWARF53 signalling and contributes to rice blast resistance.