Involvement of C-22-Hydroxylated Brassinosteroids in Auxin-Induced Lamina Joint Bending in Rice

被引:48
作者
Nakamura, Ayako [1 ]
Fujioka, Shozo [1 ]
Takatsuto, Suguru [2 ]
Tsujimoto, Masafumi [1 ]
Kitano, Hidemi [3 ]
Yoshida, Shigeo [4 ]
Asami, Tadao [1 ,5 ]
Nakano, Takeshi [1 ,6 ]
机构
[1] RIKEN, Adavanced Sci Inst, Wako, Saitama 3510198, Japan
[2] Joetsu Univ Educ, Dept Chem, Niigata 9438512, Japan
[3] Nagoya Univ, Biosci & Biotechnol Ctr, Chikusa Ku, Nagoya, Aichi 4648601, Japan
[4] RIKEN, Plant Sci Ctr, Kanagawa 2300045, Japan
[5] Univ Tokyo, Grad Sch Agr & Life Sci, Bunkyo Ku, Tokyo 1138657, Japan
[6] JST PRESTO, Kawaguchi, Saitama 3320012, Japan
基金
日本科学技术振兴机构; 日本学术振兴会;
关键词
Auxin; Brassinosteroid; Lamina joint; Rice; INCLINATION BIOASSAY; BIOSYNTHETIC-PATHWAY; BRASSINOLIDE; ARABIDOPSIS; LEAVES; CYTOCHROME-P450; MUTANT; HYDROXYLATION; DEFICIENCY; ELONGATION;
D O I
10.1093/pcp/pcp106
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
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.
引用
收藏
页码:1627 / 1635
页数:9
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