Strigolactone receptor D14 integrates phosphate and strigolactone signaling by interacting with and stabilizing PHR1

Strigolactone (SL) and low phosphate (LP) signaling coordinately regulate shoot and root architecture and plant adaptation. While LP signaling is generally considered upstream of SL biosynthesis, their interaction is more complex. For instance, exogenous SL exerts opposite effects on lateral root formation under low versus high phosphorus. Here, we show that under LP, SL-induced anthocyanin accumulation requires PHR1, demonstrating that PHR1 functions downstream of SL signaling. We uncovered an SL-dependent physical interaction between PHR1 and the SL receptor DWARF14 (D14). This interaction promotes PHR1 dimerization, stabilizes PHR1 by inhibiting its ubiquitination-mediated degradation, and enhances its transcriptional activation activity. The D14-PHR1 complex directly binds and up-regulates the SL biosynthesis gene MAX3 and anthocyanin biosynthesis genes, thereby inhibiting branching and hypocotyl elongation and promoting anthocyanin accumulation. These findings indicate that PHR1 mediates the coordination of SL and LP signaling, potentially explaining SL’s opposing effects on lateral root formation under different phosphorus conditions. In the phr1 mutant, exogenous SL inhibited lateral roots under both LP and Pi-sufficient conditions, confirming that the promoting role of SL under LP requires PHR1. PHR1 also interacted with D14 to activate LBDs and HB23 , regulating lateral root formation. Collectively, LP signaling coordinates with SL signaling via two parallel pathways: regulating SL biosynthesis to align SL functions with LP requirements and enhancing PHR1 activity through PHR1-D14 interaction to amplify LP signaling outputs.