The molecular intersection of brassinosteroid-regulated growth and flowering in Arabidopsis.

T he transition from vegetative to reproductive growth in plants is a major developmental switch regulated by a set of complex, integrated signal transduction pathways that respond to both environmental cues and endogenous signals to alter the expression of genes associated with the initiation and development of floral organs (1). Understanding the molecular mechanisms of flowering has both intrinsic scientific interest and immense practical agricultural applications. In many plants, the timing of flowering is regulated by light quality and quantity, temperature, and the action of gibberellins (GAs), a class of plant hormones with pleiotropic effects on both vegetative and reproductive development (2). Another class of plant hormones, the brassinosteroids (BRs), also regulates multiple aspects of plant development (3), and recent evidence suggests that BRs stimulate flowering by reducing transcript levels of a potent floral repressor (4). As with many other developmental processes in plants, our understanding of molecular events underlying floral initiation has been greatly advanced by studying mutants in the model plant Arabidopsis thaliana. The molecular genetic analysis of Arabidopsis mutants exhibiting early or delayed flowering has uncovered numerous critical components of signal transduction pathways regulating response to photoperiod, hormones, and cold treatment. Similarly, analysis of mutants with defective BR perception or response has provided extensive details on the molecular components required for BR signaling (5, 6). In this issue of PNAS, Yu et al. (7) provide a connection between BR signal transduction and pathways controlling floral initiation by demonstrating that a critical transcription factor required for BRdependent gene expression directly interacts with two transcription regulators previously identified as having divergent roles in modulating time of flowering in Arabidopsis (8). BRs have structural similarities to animal steroid hormones and initiate a cascade of cellular events by binding to the extracellular domain of the BRASSINOSTEROID-INSENSITIVE 1 (BRI1) receptor kinase (5). This leads to phosphorylation of the BRI1 cytoplasmic kinase domain, causing disassociation from the membrane-bound BRI1 KINASE INHIBITOR 1 (BKI1) and oligomerization with a second receptor kinase, BRI1-ASSOCIATED RECEPTOR KINASE 1 (BAK1). The active BRI1/BAK1 receptor kinase pair then propagates the signal downstream by inactivating a soluble kinase, BRASSINOSTEROID-INSENSITIVE 2 (BIN2), which is a negative regulator of BR signaling (6). Mutational analysis in Arabidopsis reveals that bri1 null alleles have severe developmental defects, including extreme dwarfism, altered leaf and vascular morphology, delayed senescence, male infertility, and moderately delayed flowering, confirming the importance of BRI1-mediated BR signaling in normal plant development (3, 6).