Lesions in the sterol Delta(7) reductase gene of Arabidopsis cause dwarfism due to a block in brassinosteroid biosynthesis

Citation
S. Choe et al., Lesions in the sterol Delta(7) reductase gene of Arabidopsis cause dwarfism due to a block in brassinosteroid biosynthesis, PLANT J, 21(5), 2000, pp. 431-443
Citations number
51
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
PLANT JOURNAL
ISSN journal
0960-7412 → ACNP
Volume
21
Issue
5
Year of publication
2000
Pages
431 - 443
Database
ISI
SICI code
0960-7412(200003)21:5<431:LITSDR>2.0.ZU;2-G
Abstract
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 A rabidopsis. Here we show that the Arabidopsis dwarf5 mutants are disrupted in a sterol Delta(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. Metabo lite tracing with C-13-labeled precursors in dwf5 verified a deficiency in a sterol Delta(7) reductase activity. All six independent alleles contain t oss-of-function mutations in the sterol Delta(7) reductase gene. These incl ude a putative mRNA instability mutation in dwf5-1, 3' and 5' splice-site m utations 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). T he dwf5 plant could be restored to wild type by ectopic overexpression of t he 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 i n a sterol Delta(7) reductase gene, indicating that it is required for the proper growth and development of these two organisms.