Strigolactone/MAX2-Induced Degradation of Brassinosteroid Transcriptional Effector BES1 Regulates Shoot Branching

•BES1 protein accumulation leads to enhanced rosette branching and SL insensitivity•BES1 interacts with an F box protein, MAX2, and serves as a substrate of MAX2•MAX2-mediated BES1 degradation is promoted by SLs•Reduced expression of BES1 greatly suppresses branching phenotype of max2-1

SummaryStrigolactones (SLs), a class of the most recently identified terpenoid phytohormones, play essential roles in plant development, specifically in suppressing shoot branching. MAX2, a subunit of an SCF E3 ligase and a positive regulator that inhibits shoot branching, is likely a key SL signaling component. Here, we provide genetic and biochemical evidence to demonstrate that BES1 interacts with MAX2 and acts as its substrate to regulate SL-responsive gene expression. Additional AtD14, a putative receptor of SLs, can promote BES1 degradation. Knockdown of BES1 and its homologs dramatically suppressed the branching phenotype of max2-1 mutant. These results portray an SL signaling cascade from the putative receptor to downstream transcription factors. In addition, we demonstrate that the SL and brassinosteroid (BR) signaling pathways distinctly regulate the same transcription factor, BES1, to control specific developmental processes.

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