Abstract:
:The cpd mutation localized by T-DNA tagging on Arabidopsis chromosome 5-14.3 inhibits cell elongation controlled by the ecdysone-like brassinosteroid hormone brassinolide. The cpd mutant displays de-etiolation and derepression of light-induced genes in the dark, as well as dwarfism, male sterility, and activation of stress-regulated genes in the light. 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 brassinolide precursors and by ectopic overexpression of the CPD cDNA. Brassinosteroids also compensate for different cell elongation defects of Arabidopsis det, cop, fus, and axr2 mutants, indicating that these steroids play an essential role in the regulation of plant development.
journal_name
Celljournal_title
Cellauthors
Szekeres M,Németh K,Koncz-Kálmán Z,Mathur J,Kauschmann A,Altmann T,Rédei GP,Nagy F,Schell J,Koncz Cdoi
10.1016/s0092-8674(00)81094-6subject
Has Abstractpub_date
1996-04-19 00:00:00pages
171-82issue
2eissn
0092-8674issn
1097-4172pii
S0092-8674(00)81094-6journal_volume
85pub_type
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