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BEN1 , a gene encoding a dihydroflavonol 4‐reductase (DFR)‐like protein, regulates the levels of brassinosteroids in Arabidopsis thaliana
Author(s) -
Yuan Tong,
Fujioka Shozo,
Takatsuto Suguru,
Matsumoto Shogo,
Gou Xiaoping,
He Kai,
Russell Scott D.,
Li Jia
Publication year - 2007
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2007.03129.x
Subject(s) - brassinosteroid , mutant , arabidopsis thaliana , biology , arabidopsis , brassinolide , gene , genetics , wild type , reductase , microbiology and biotechnology , biochemistry , enzyme , botany , plant growth
Summary The ben1‐1D ( b ri1‐5 en hanced 1 ‐ 1d ominant) mutant was identified via an activation‐tagging screen for bri1‐5 extragenic modifiers. bri1‐5 is a weak mutant allele of the brassinosteroid receptor gene, BRI1 . Overexpression of BEN1 greatly enhances the defective phenotypes of bri1‐5 plants. Removal of BEN1 by gene disruption in a Col‐0 wild‐type background, on the other hand, promotes the elongation of organs. Because BEN1 encodes a novel protein homologous to dihydroflavonol 4‐reductase (DFR) and anthocyanidin reductase (BAN), BEN1 is probably involved in a brassinosteroid metabolic pathway. Analyses of brassinosteroid profiles demonstrated that BEN1 is indeed responsible for regulating the levels of several brassinosteroids, including typhasterol, castasterone and brassinolide. In vivo feeding and in vitro biochemical assays suggest that BEN1 is probably involved in a new mechanism to regulate brassinosteroid levels. These results provide additional insight into the regulatory mechanisms of bioactive brassinosteroids.