Brassinosteroid homeostasis via coordinate regulation of signaling and synthetic pathways.

A widely accepted regulatory mechanism in maintaining hormone homeostasis involves negative or positive feedback control of biosynthetic genes through signal transduction pathways triggered by hormones. For brassinosteroid (BR) homeostasis, the antagonistic relationship between signaling and biosynthetic pathways has been well characterized. We have identified a transcriptional regulator, RAV-Like1, which activates both a BR receptor gene (BRI1) and BR synthetic genes (D2, D11, and BRD1). RAVL1 possesses a B3 DNA binding domain that exhibits differential affinity for E-box elements in the promoters of BRI1, D2, D11, and BRD1. Semi-dwarfism and BR-insensitive phenotypes are exhibited by ravl1 mutants. Genetic studies have demonstrated that expression alteration of BRI1 and BR synthetic genes by RAVL1 results in changes in BR sensitivity. BZR1 is a negative regulator involved in BR feedback mechanisms. To examine the relationship between RAVL1 and BZR1, expression of the common target gene BRD1 was examined using a transient transcription assay. The suppression of BRD1 by BZR1 is epistatic to activation by RAVL1. More importantly, RAVL1 is not subject to BR feedback regulation. Taken together, this data indicates that RAVL1 is involved in maintaining the basal activity of BRI1 and BR synthetic genes, which ensures that the basal levels of the hormone are produced. This study elucidated the RAVL1-mediated basal activation system which, in cooperation with negative feedback mechanisms, maintains BR homeostasis in higher plants.