Biosynthesis and Inactivation of Brassinosteroids in Plants

Abstract

Brassinosteroid (BRs) biosynthetic pathways have been well studied in genetic approaches. BRs contain 27, 28, or 29 carbons within their skeletal structure: 5α-cholestane, 5α-ergostane, or 5α-stigmastane. BRs are derived from sterols carrying the same side chain. C27-BRs without a substituent at C-24 are biosynthesized from cholesterol. C28-BRs carrying either an α-methyl, β-methyl, or methylene group are derived from campesterol, 24-epicampesterol, or 24-methylenecholesterol, respectively. C29-BRs with an α-ethyl group are produced from sitosterol, while those carrying methylene at C-24 and an additional methyl group at C-25 are derived from 24-methylene-25-methylcholesterol. Generally, BRs are biosynthesized via cycloartenol and cycloartanol-dependent pathways. Until now, more than 17 inhibitors of BR biosynthesis, nine of which (e.g., brassinazole and YCZ-18) have a specific target reaction identified within the BR biosynthetic pathway. Besides biosynthesis, BR catabolism is an important process regulating the endogenous level of BRs. Biochemical reactions involved in BR metabolism and inactivation include dehydrogenation, demethylation, epimerization, esterification, glycosylation, hydroxylation, side-chain cleavage, and sulfonation. Most of the catabolic changes were described for brassinolide, castasterone, 24-epibrassinolide, and 24-epiteasterone. Genetic regulation of metabolism species of plants has also been examined. The crucial role in these processes is played by P450 monooxygenases. Overexpression of genes involved in BR inactivation significantly reduces BR content. Analyses of BR-deficient mutants indicated the strong inhibition of plant growth and development. Moreover, exogenously applied inactive metabolites of BRs do not affect their phenotype, in contrast to active BRs, which cause considerable plant growth.