Document Type

Technical Report

Date of this Version

3-1999

Publication Source

Plant Physiology

Volume

119

Issue

3

Start Page

897

Last Page

907

DOI

10.1104/pp.119.3.897

Abstract

Since the isolation and characterization of dwarf1-1 (dwf1-1) from a T-DNA insertion mutant population, phenotypically similar mutants, including deetiolated2 (det2),constitutive photomorphogenesis and dwarfism(cpd), brassinosteroid insensitive1 (bri1), and dwf4, have been reported to be defective in either the biosynthesis or the perception of brassinosteroids. We present further characterization of dwf1-1 and additional dwf1 alleles. Feeding tests with brassinosteroid-biosynthetic intermediates revealed that dwf1 can be rescued by 22α-hydroxycampesterol and downstream intermediates in the brassinosteroid pathway. Analysis of the endogenous levels of brassinosteroid intermediates showed that 24-methylenecholesterol in dwf1 accumulates to 12 times the level of the wild type, whereas the level of campesterol is greatly diminished, indicating that the defective step is in C-24 reduction. Furthermore, the deduced amino acid sequence of DWF1 shows significant similarity to a flavin adenine dinucleotide-binding domain conserved in various oxidoreductases, suggesting an enzymatic role for DWF1. In support of this, 7 of 10 dwf1 mutations directly affected the flavin adenine dinucleotide-binding domain. Our molecular characterization of dwf1 alleles, together with our biochemical data, suggest that the biosynthetic defect in dwf1 results in reduced synthesis of bioactive brassinosteroids, causing dwarfism.

Copyright/Permission Statement

Copyright © 1999 American Society of Plant Physiologists. Reproduced with permission.

Comments

At the time of this publication, Dr. Gregory was affiliated with the University of Arizona, but he is now a faculty member at the University of Pennsylvania.

 

Date Posted: 14 July 2017

This document has been peer reviewed.