A novel mutant allele uncouples brassinosteroid-dependent and independent functions of BRI1

Plants depend on an array of cell surface receptors to integrate extracellular signals with developmental programs. One of the best-studied receptors is BRASSINOSTEROID INSENSITIVE 1 (BRI1), which upon binding of its hormone ligands forms a complex with shape-complimentary co-receptors and initiates a signal transduction cascade leading to a wide range of responses. BR biosynthetic and receptor mutants have similar growth defects on the macroscopic level, which had initially led to the assumption of a largely linear signalling pathway. However, recent evidence suggests that BR signalling is interconnected with a number of other pathways through a variety of different mechanisms. We recently described that feedback information from the cell wall is integrated at the level of the receptor complex through interaction with RLP44. Moreover, BRI1 is required for a second function of RLP44, the control of procambial cell fate. Here, we report on a BRI1 mutant, bri1cnu4, which differentially affects canonical BR signalling and RLP44 function in the vasculature. While BR signalling is only mildly impaired, bri1cnu4 mutants show ectopic xylem in the position of procambium. Mechanistically, this is explained by an increased association of RLP44 and the mutated BRI1 protein, which prevents the former from acting in vascular cell fate maintenance. Consistent with this, the mild BR response phenotype of bri1cnu4 is a recessive trait, whereas the RLP44-mediated xylem phenotype is semi-dominant. Our results highlight the complexity of plant plasma membrane receptor function and provide a tool to dissect BR signalling-related roles of BRI1 from its non-canonical functions.