The Arabidopsis dwf7/ste1 mutant is defective in the Δ7 sterol C-5 desaturation step leading to brassinosteroid biosynthesis

被引:205
作者
Choe, SW
Noguchi, T
Fujioka, S
Takatsuto, S
Tissier, CP
Gregory, BD
Ross, AS
Tanaka, A
Yoshida, S
Tax, FE
Feldmann, KA [1 ]
机构
[1] Univ Arizona, Dept Plant Sci, Tucson, AZ 85721 USA
[2] RIKEN, Inst Phys & Chem Res, Wako, Saitama 3510198, Japan
[3] Joetsu Univ Educ, Dept Chem, Joetsu, Niigata 9438512, Japan
[4] Japan Atom Energy Res Inst, Dept Environm & Resources, Takasaki, Gumma 3701292, Japan
关键词
D O I
10.1105/tpc.11.2.207
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Lesions in brassinosteroid (BR) biosynthetic genes result in characteristic dwarf phenotypes in plants. Understanding the regulation of BR biosynthesis demands continued isolation and characterization of mutants corresponding to the genes involved in BR biosynthesis. Here, we present analysis of a novel BR biosynthetic locus, dwarf7 (dwf7). Feeding studies with BR biosynthetic intermediates and analysis of endogenous levels of BR and sterol biosynthetic intermediates indicate that the defective step in dwf7-1 resides before the production of 24-methylenecholesterol in the sterol biosynthetic pathway. Furthermore, results from feeding studies with C-13-labeled mevalonic acid and compactin show that the defective step is specifically the Delta(7) sterol C-5 desaturation, suggesting that dwf7 is an allele of the previously cloned STEROL1 (STE1) gene. Sequencing of the STE1 locus in two dwf7 mutants revealed premature stop codons in the first (dwf7-2) and the third (dwf7-1) exons. Thus, the reduction of BRs in dwn is due to a shortage of substrate sterols and is the direct cause of the dwarf phenotype in dwf7.
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收藏
页码:207 / 221
页数:15
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