Lesions in the sterol Δ7 reductase gene of Arabidopsis cause dwarfism due to a block in brassinosteroid biosynthesis

Sunghwa Choe, Atsushi Tanaka, Takahiro Noguchi, Shozo Fujioka, Suguru Takatsuto, Amanda S. Ross, Frans E. Tax, Shigeo Yoshida, Kenneth A. Feldmann

Research output: Contribution to journalArticlepeer-review

114 Scopus citations

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 Arabidopsis. Here we show that the Arabidopsis dwarf5 mutants are disrupted in a sterol Δ7 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 13C-labeled precursors in dwf5 verified a deficiency in a sterol Δ7 reductase activity. All six independent alleles contain loss-of-function mutations in the sterol Δ7 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 Δ7 reductase gene, indicating that it is required for the proper growth and development of these two organisms.

Original languageEnglish (US)
Pages (from-to)431-443
Number of pages13
JournalPlant Journal
Volume21
Issue number5
DOIs
StatePublished - Mar 1 2000

ASJC Scopus subject areas

  • Genetics
  • Plant Science
  • Cell Biology

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