Involvement of C-22-hydroxylated brassinosteroids in auxin-induced lamina joint bending in rice.

The rice lamina joint is ideal material for investigating the activity of brassinosteroids (BRs) and auxin because of its high sensitivity to these compounds. Using a series of rice BR biosynthetic and receptor mutants, we conducted lamina joint tests to elucidate the mechanism of cross-talk between BR and auxin signaling in lamina joint bending. In BR biosynthetic mutants d2 and brd1, which are defective in C-23 hydroxylase and C-6 oxidase, respectively, the lamina joint response to auxin was significantly higher than that of wild-type plants. The other BR-biosynthetic mutants, brd2, osdwarf4 and d11, which are defective in C-22-hydroxylated BRs, showed less or no response to auxin. These results suggest that C-22-hydroxylated BRs are involved in auxin-induced lamina joint bending. The results were supported by the observation that inhibition of the hyper-response to auxin in d2 was reduced by treatment with brassinazole, which inhibits the function of DWARF4, the C-22 hydroxylase. In d61, which is defective in OsBRI1, a possible BR receptor in rice, the bending angle of the lamina joint in response to auxin and C-22-hydroxylated 6-deoxoBRs was nearly the same as that in wild-type plants. This implies that C-22-hydroxylated BRs function in auxin signaling independently of OsBRI1. From these observations, we propose that C-22-hydroxylated BRs participate in auxin signaling via a novel OsBRI1-independent signaling pathway.