Fig. 3. bri1 mutant plants and signaling. (A) Representation of wild type and the severe dwarf phenotype observed in bri1 mutant plants. Rosette leaves of bri1 plants are `cabbage-like', because of defects in stem elongation, and cell expansion of hypocotyls and petioles. (B) Model for the BRI1 signaling pathway. The type II serine carboxypeptide BRS1 activates a putative steroid binding protein (proSBP), which then associates with the brassinosteriod BR. SBP-BR interacts with the LRR-RLK BRI1 (red) and the receptor BAK1 (dark blue). BAK1/BRI1 then inactivate the GSK3-like kinase BIN2, which is an upstream regulator of BES1 and BRZ1. In the absence of BR, BIN2 is constitutively active, and phosphorylates BES1 and BRZ1, leading to their degradation. When BES1 and BRZ1 are not phosphorylated, they are localized to the nucleus where they activate transcription of brassinosteroid responsive genes.