Strigolactone-Induced Degradation Of BES1 Regulates Shoot Branching

Strigolactones (SLs) are new terpenoid plant hormones, which were originally discovered as stimulitants for germination of parasite weeds. However, recent studies demonstrate that SLs coordinate with Auxin and cytokinins to modulate the development of plant lateral branches and shape the plant. SLs are derived from β-carotene and sequentiallyproceeded by carotenoid cleavage dioxygenase 7 and 8, as well as cytochrome to form a kind of movable and active compounds. In other hand, it has been identified that two critical components are involved in SL signal pathway, including receptor AtD14/DAD2/D14 and an F-box protein MAX2/RMS4/D3. Due to the AtD14 encodes an α/β-fold hydrolase, and MAX2 protein as a subunit participates the SCF (S phase kinase-associated protein 1-cullin-F box) complex, which is largely reminiscent of gibberellin(GA) signaling pathway. Thus, previous studies proposed a putative model of SL signal transduction, in which SL binding to AtD14 facilitates the degradation of substrate by MAX2 to inhibit the shoot branching. However, the substrate of MAX2 and the actual mechanism of SL signal transduction are still to be characterized.In this study, we found a gain of function mutant of an essential transcriptional effector in brassinosteroid (BR) signal pathway, besl-D, has more rosette branches and longer hypocotyl, which are similar to a loss of function mutant of MAX2. In addition, the besl-D mutant also exhibits similar SL insensitivity in inhibition of shoot branching and hypocotyl elongation with max2-1. Through screening the MAX2 interacting protein, we found MAX2 is able to interact with BES1 family protein, and both phosphorylated and dephosphorylated BES1 can be associated with MAX2. The further ubiquitination assay and cell free degradation assay showed that MAX2 is required for the ubiquitination and degradation of BES1. Moreover, the SL receptor also mediates the BES1 degradation. However, unlike the GA signal pathway, SL doesn’t enhance the interaction between MAX2 and BES1, but promotes the MAX2-dependent degradation of BES1 protein. We also construct the BES1-RNAi/max2-1 double mutant and found that depletion of BES1 and its homologues would suppress shoot branchingof max2-1. These evidences suggest that BES1 protein acts as a negative component downstream of MAX2 to deliver the SL signal.This study established an SL signaling cascade from the putative receptor to downstream transcription factors, paving the way for deeply understanding mechanism of how the SLs regulate the plant growth and development and improving the crop traits. In addition, we demonstrated that the SLs and BRs signaling pathways distinctly regulate the same transcription factor, BES1, to control specific developmental processes.