The strigolactone receptor D14 targets SMAX1 for degradation in response to GR24 treatment and osmotic stress.

The effects of the phytohormone strigolactone (SL) and smoke-derived karrikins (KARs) on plants are generally distinct, despite the fact that they are perceived through very similar mechanisms. The homologous receptors DWARF14 (D14) and KARRIKIN-INSENSITIVE2 (KAI2), together with the F-box protein MORE AXILLARY GROWTH2 (MAX2), mediate SL and KAR responses, respectively, by targeting different SMAX1-LIKE (SMXL) family proteins for degradation. These mechanisms are putatively well-insulated, with D14-MAX2 targeting SMXL6, SMXL7, and SMXL8 and KAI2-MAX2 targeting SMAX1 and SMXL2 in . Recent evidence challenges this model. We investigated whether D14 can target SMAX1 and whether this occurs naturally. Genetic analysis indicates that the SL analog GR24 promotes D14-SMAX1 crosstalk. Although D14 shows weaker interactions with SMAX1 than with SMXL2 or SMXL7, D14 mediates GR24-induced degradation of SMAX1 in plants. Osmotic stress triggers SMAX1 degradation, which is protective, through SL biosynthesis and signaling genes. Thus, D14-SMAX1 crosstalk may be beneficial and not simply a vestige of the evolution of the SL pathway.