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First published online 4 July 2007
doi: 10.1242/dev.02866


Development 134, 2841-2850 (2007)
Published by The Company of Biologists 2007


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Attenuation of brassinosteroid signaling enhances FLC expression and delays flowering

Malgorzata A. Domagalska1, Fritz M. Schomburg2, Richard M. Amasino2, Richard D. Vierstra3, Ferenc Nagy4 and Seth J. Davis1,*

1 Max Planck Institute for Plant Breeding Research, Carl-von-Linné-Weg 10, 50829 Cologne, Germany.
2 Department of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA.
3 Laboratory of Genetics, University of Wisconsin-Madison, Madison, WI 53706, USA.
4 Institute of Plant Biology, Biological Research Centre, Hungarian Academy of Science, Szeged, Hungary.

* Author for correspondence (e-mail: davis{at}mpiz-koeln.mpg.de)

Accepted 8 May 2007

A main developmental switch in the life cycle of a flowering plant is the transition from vegetative to reproductive growth. In Arabidopsis thaliana, distinct genetic pathways regulate the timing of this transition. We report here that brassinosteroid (BR) signaling establishes an unexpected and previously unidentified genetic pathway in the floral-regulating network. We isolated two alleles of brassinosteroid-insensitive 1 (bri1) as enhancers of the late-flowering autonomous-pathway mutant luminidependens (ld). bri1 was found to predominantly function as a flowering-time enhancer. Further analyses of double mutants between bri1 and known flowering-time mutants revealed that bri1 also enhances the phenotype of the autonomous mutant fca and of the dominant FRI line. Moreover, all of these double mutants exhibited elevated expression of the potent floral repressor FLOWERING LOCUS C (FLC). This molecular response could be efficiently suppressed by vernalization, leading to accelerated flowering. Additionally, specific reduction of the expression of FLC via RNA interference accelerated flowering in bri1 ld double mutants. Importantly, combining the BR-deficient mutant cpd with ld also resulted in delayed flowering and led to elevated FLC expression. Finally, we found increased histone H3 acetylation at FLC chromatin in bri1 ld mutants, as compared with ld single mutants. In conclusion, we propose that BR signaling acts to repress FLC expression, particularly in genetic situations, with, for example, dominant FRI alleles or autonomous-pathway mutants, in which FLC is activated.

Key words: Brassinosteroid, Flowering time, BRI1, FLC, Autonomous pathway, luminidependens, Arabidopsis thaliana


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