RALF33–FERONIA signaling orchestrates postwounding root-tip regeneration via TPR4–ERF115 dynamics

Abstract

The molecular mechanisms underlying wound-induced tissue and organ regeneration in plants are unclear. Here, we identified a signaling pathway that governs the wound-induced regeneration of Arabidopsis (Arabidopsis thaliana) roots, highlighting a key role for the peptide RAPID ALKALINIZATION FACTOR33 (RALF33) and its receptor FERONIA (FER). Wounding triggers RALF33 accumulation, which promotes root regeneration, and fer mutants exhibit an enhanced regeneration capacity. The accumulated RALF33 hinders FER-mediated phosphorylation of the transcriptional co-repressor TOPLESS-RELATED4 (TPR4), impairing TPR4 nuclear localization and inhibiting its interaction with the transcription factor ETHYLENE RESPONSE FACTOR115 (ERF115). ERF115 has greater transcriptional activity when it is not associated with TPR4. Disrupting the FER-targeted phosphorylation sites in TPR4 via alanine substitutions (TPR4A) resulted in TPR4 mislocalization and impaired binding of TPR4A to ERF115. Our findings reveal that RALF33-FER-TPR4-ERF115 compose a key signaling cascade that orchestrates wound-induced regeneration, providing valuable insights into the regulation of plant regenerative responses.