Crosstalk Between Phosphorylation and Ubiquitination Controls the Fate and Function of Strigolactone Signal Transducers

Abstract Strigolactones (SL) are pivotal plant hormones that sculpt plant architecture by modulating shoot branching, root development, and meristem activity. While transcriptional responses downstream of SL perception have been well explored, the role of post-translational regulation fine-tuning these responses remains less understood. In this study, we identify a dual-layered regulatory module involving MPK4-mediated phosphorylation and MAX2-dependent ubiquitination that synergistically control the stability and function of BRC1, a key SL-responsive transcription factor. Phosphorylation by MPK4 stabilizes BRC1, enhancing its activity and SL sensitivity, whereas loss of phosphorylation leads to BRC1 degradation and functional inactivation. BRC1, in turn, directly activates MPK4 transcription, establishing a positive feedback loop that amplifies SL signaling. Genetic analyses of the brc1-2 × mpk4 double mutant reveals phenotypic defects and SL insensitivity additive to those observed in the brc1-2 and mpk4 single mutants, indicating that MPK4 and BRC1 act in parallel yet converging pathways downstream of SL. Additionally, MAX2 functions as a regulatory checkpoint that degrades non-phosphorylated MPK4 and BRC1, thereby resetting the signaling circuit to ensure accurate and timely response. Together, these findings illuminate a finely-tuned regulatory module integrating phosphorylation and ubiquitination to control the intensity and duration of SL responses, suggesting a model for hormone-driven developmental plasticity in plants. Competing Interest Statement The authors have declared no competing interest.