BRASSINOSTEROID-INDUCED DE-ETIOLATION OF ARABIDOPSIS-THALIANA SEEDLINGS RESEMBLES THE LONG-TERM EFFECTS OF CYTOKININS

Citation
J. Luo et al., BRASSINOSTEROID-INDUCED DE-ETIOLATION OF ARABIDOPSIS-THALIANA SEEDLINGS RESEMBLES THE LONG-TERM EFFECTS OF CYTOKININS, Australian journal of plant physiology, 25(6), 1998, pp. 719-728
Citations number
35
Categorie Soggetti
Plant Sciences
ISSN journal
03107841
Volume
25
Issue
6
Year of publication
1998
Pages
719 - 728
Database
ISI
SICI code
0310-7841(1998)25:6<719:BDOAS>2.0.ZU;2-7
Abstract
Cytokinins can cause de-etiolation of Arabidopsis thaliana (L.) Heynh. seedlings growing in the dark. Brassinosteroids (BRs) have been consi dered to regulate negatively the de-etiolation in dark-grown Arabidops is seedlings. We show here that epi-brassinolide (epi-BL) can partiall y produce the phenotype of de-etiolation as caused by treatment with c ytokinins in the dark, including the development of leaves and epicoty ls in the wild-type and the BR-deficient mutant det2. But BRs cannot i nhibit hypocotyl elongation, nor restore all the inhibition caused by cytokinins and light. We have found that there are distinct short term and long term phases of induction of de-etiolation by cytokinins. The shortterm effect is probably coupled to ethylene in the inhibition of the hypocotyl elongation; the long-term effect causes morphogenesis o f leaves and epicotyls. BRs can only regulate de-etiolation in the lon g term. We propose that the inhibition of hypocotyl elongation of det2 in darkness is caused by the absence of BR-dependent elongation rathe r than the inhibition caused by the expression of genes for photomorph ogenesis. We propose that BRs resemble cytokinins in regulating de-eti olation as positive regulators, and that the inhibition of hypocotyl e longation and the development of leaves and epicotyls in de-etiolation are independent processes.