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Lesions in the sterol Δ 7 reductase gene of Arabidopsis cause dwarfism due to a block in brassinosteroid biosynthesis
Author(s) -
Choe Sunghwa,
Tanaka Atsushi,
Noguchi Takahiro,
Fujioka Shozo,
Takatsuto Suguru,
Ross Amanda S.,
Tax Frans E.,
Yoshida Shigeo,
Feldmann Kenneth A.
Publication year - 2000
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 - 10.1046/j.1365-313x.2000.00693.x
Subject(s) - arabidopsis , biology , mutant , sterol , genetics , brassinosteroid , gene , reductase , phenotype , arabidopsis thaliana , mutation , biochemistry , enzyme , cholesterol
Summary The brassinosteroid (BR) biosynthetic pathway, and the sterol pathway which is prerequisite to the BR pathway, are rapidly being characterized because of the availability of a large number of characteristic dwarf mutants in Arabidopsis. Here we show that the Arabidopsis dwarf5 mutants are disrupted in a sterol Δ 7 reduction step. dwf5 plants display the characteristic dwarf phenotype typical of other BR mutants. This phenotype includes small, round, dark‐green leaves, and short stems, pedicels, and petioles. Metabolite tracing with 13 C‐labeled precursors in dwf5 verified a deficiency in a sterol Δ 7 reductase activity. All six independent alleles contain loss‐of‐function mutations in the sterol Δ 7 reductase gene. These include a putative mRNA instability mutation in dwf5‐1, 3′ and 5′ splice‐site mutations in dwf5‐2 and dwf5‐6 , respectively, premature stop codons in dwf5‐3 (R400Z) and dwf5‐5 (R409Z), and a mis‐sense mutation in dwf5‐4 (D257N). The dwf5 plant could be restored to wild type by ectopic overexpression of the wild‐type copy of the gene. Both the Arabidopsis dwf5 phenotype and the human Smith–Lemli–Opitz syndrome are caused by loss‐of‐function mutations in a sterol Δ 7 reductase gene, indicating that it is required for the proper growth and development of these two organisms.