Fig. 8.

A working model for a negative feedback mechanism that controls BRI1 abundance and BR signaling. (A) In the absence of BRs, inactive BRI1 molecules are constitutively internalized and recycled between the endosomes and the plasma membrane. (B) Binding of BRs by BRI1 at the cell surface leads to BRI1 activation and phosphorylation. Activated BRI1 initiates the BR signaling cascade, including the induction of SBI1 transcription. SBI1 methylates and targets PP2A to the endosomes, which in turn dephosphorylates BRI1. Dephosphorylated BRI1 molecules are then degraded (possibly in the vacuole), thus terminating BR signaling. A question mark represents a process that is postulated to occur, but has not been shown. Our model indicates BR signaling is initiated from the cell surface, but this model would not exclude the possibility that BR signaling can be initiated from intra-cellular membranous compartments. For simplicity, other components of the pathway, such as BAK1, BSK1, BKI1, BIN2, BES1, BZR1, and BSU1, are not shown.