BRASSINOSTEROIDS RESCUE THE DEFICIENCY OF CYP90, A CYTOCHROME-P450, CONTROLLING CELL ELONGATION AND DE-ETIOLATION IN ARABIDOPSIS

The cpd mutation localized by T-DNA tagging on Arabidopsis chromosome 5-14.3 inhibits cell elongation controlled by the ecdysone-like brassi nosteroid hormone brassinolide. The cpd mutant displays de-etiolation and derepression of light-induced genes in the dark, as well as dwarfi sm, male sterility, and activation of stress-regulated genes in the li ght. The CPD gene encodes a cytochrome P450 (CYP90) sharing homologous domains with steroid hydroxylases. The phenotype of the cpd mutant is restored to wild type both by feeding with C23-hydroxylated brassinol ide precursors and by ectopic overexpression of the CPD cDNA. Brassino steroids also compensate for different cell elongation defects of Arab idopsis dot, cop, fus, and axr2 mutants, indicating that these steroid s play an essential role in the regulation of plant development.