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DEVELOPMENT AND HORMONE ACTION

Brassinosteroid Homeostasis in Arabidopsis Is Ensured by Feedback Expressions of Multiple Genes Involved in Its Metabolism

Department of Agricultural Sciences and Natural Resources (K.T., S.O.), and Department of Biochemical Science and Technology (T.M.), Kagoshima University, Kagoshima 890–0065, Japan; Institute of Physical and Chemical Research, Wako, Saitama 351–0198, Japan (T.A., S.Y.); and Department of Food Science and Nutritional Health, Kyoto Prefectural University, Sakyo-ku, Kyoto 606–8522, Japan (Y.N.)

Homeostasis of brassinosteroids (BRs) is essential for normal growth and development in higher plants. We examined responsiveness of 11 BR metabolic gene expressions to the decrease or increase of endogenous BR contents in Arabidopsis (Arabidopsis thaliana) to expand our knowledge of molecular mechanisms underlying BR homeostasis. Five BR-specific biosynthesis genes (DET2, DWF4, CPD, BR6ox1, and ROT3) and two sterol biosynthesis genes (FK and DWF5) were up-regulated in BR-depleted wild-type plants grown under brassinazole, a BR biosynthesis inhibitor. On the other hand, in BR-excessive wild-type plants that were fed with brassinolide, four BR-specific synthesis genes (DWF4, CPD, BR6ox1, and ROT3) and a sterol synthesis gene (DWF7) were down-regulated and a BR inactivation gene (BAS1) was up-regulated. However, their response to fluctuation of BR levels was highly reduced (DWF4) or nullified (the other eight genes) in a bri1 mutant. Taken together, our results imply that BR homeostasis is maintained through feedback expressions of multiple genes, each of which is involved not only in BR-specific biosynthesis and inactivation, but also in sterol biosynthesis. Our results also indicate that their feedback expressions are under the control of a BRI1-mediated signaling pathway. Moreover, a weak response in the mutant suggests that DWF4 alone is likely to be regulated in other way(s) in addition to BRI1 mediation.

^* Corresponding author; e-mail okamoto{at}agri.kagoshima-u.ac.jp; fax 81–99–285–6014.

Received December 14, 2004; returned for revision February 15, 2005; accepted February 15, 2005.

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