The FERONIA-RESPONSIVE TO DESICCATION 26 module regulates vascular immunity to <i>Ralstonia solanacearum</i>

Some pathogens colonize plant leaves, but others invade the roots, including the vasculature, causing severe disease symptoms. Plant innate immunity has been extensively studied in leaf pathosystems; however, the precise regulation of immunity against vascular pathogens remains largely unexplored. We previously demonstrated that loss of function of the receptor kinase FERONIA (FER) increases plant resistance to the typical vascular bacterial pathogen Ralstonia solanacearum. Here, we show that upon infection with R. solanacearum, root xylem cell walls in Arabidopsis thaliana become highly lignified. FER is specifically upregulated in the root xylem in response to R. solanacearum infection, and inhibits lignin biosynthesis and resistance to this pathogen. We determined that FER interacts with and phosphorylates the transcription factor RESPONSIVE TO DESICCATION 26 (RD26), leading to its degradation. Overexpression and knockout of RD26 demonstrated that it positively regulates plant resistance to R. solanacearum by directly activating the expression of lignin-related genes. Tissue-specific expression of RD26 in the root xylem confirmed its role in vascular immunity. We confirmed that the FER-RD26 module regulates lignin biosynthesis and resistance against R. solanacearum in tomato (Solanum lycopersicum). Taken together, our findings unveil that the FER-RD26 cascade governs plant immunity against R. solanacearum in vascular tissues by regulating lignin deposition. This cascade may represent a key defense mechanism against vascular pathogens in plants.