The regulation of brassinosteroid biosynthesis

Brassinosteroids (BRs) are plant-specific steroid hormones that play an essential role in plant growth and development. BRs regulate the expression of numerous genes, contribute to cell division and differentiation and help to control overall developmental programmes leading to morphogenesis. The analysis of mutants impaired in BR biosynthesis or BR perception/signaling emphasises the importance of these phytohormones in development. BR mutants of Arabidopsis thaliana grown in light are severe dwarfs with a characteristic leave morphology and also exhibit reduced fertility and apical dominance. Grown in the dark many of these mutants display a light-grown phenotype such as de-etiolation and lack of normal skotomorphogenesis, suggesting a potential interaction between BRs and light signaling pathways. Whereas BR biosynthesis has been characterised in much detail BR signal-transduction events, linking the hormone to its many biological effects, are not as well understood. The current model of BR signaling suggests that BRs are perceived by the cell surface receptor kinase BRI1, which triggers a signaling cascade that ultimately involves the dephosphorylation and accumulation in the nucleus of two transcriptional modulators BES1 and BRZ1, which regulate BR target-gene expression. BR-homeostasis is regulated via multiple mechanisms. These include inactivation, such as hydroxylation and glucosylation, and through the precise control of BR biosynthesis. To date the factors that regulate BR biosynthesis are unknown, with the only exception of BZR1, that is thought to mediate both downstream BR-responses, as well as play a part in in the feedback regulation of BR biosynthesis. I have recently identified a novel Arabidopsis mutant, cesta (ces), in which a BR over-accumulation phenotype correlates with an increase in late-pathway BRs and an altered expression of genes involved in BR biosynthesis. The ces mutant phenotype is caused by constitutive over-expression of a transcription factor. Using a complementary set of approaches the research proposed in this application aims to verify the current hypothesis that CES regulates BR biosynthesis. In addition I intend to conduct a screen of Arabidopsis mutants to identify new mechanisms that control BR biosynthesis in this model plant. The research will provide the essential foundation for revealing the role of CES in BR metabolism in Arabidopsis and will contribute to our understanding of the regulation of BR homeostasis.