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Letter
Nature 443, 458-461 (28 September 2006) | doi:10.1038/nature05130; Received 8 June 2006; Accepted 24 July 2006
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Postdoctoral Fellow - Computational Genomics - Team 78 – Ref: 80464
- Wellcome Trust Sanger Institute
- Hinxton, Cambridgeshire CB10 1, UK
Postdoctoral Research in Functional Genomics
- Harvard School of Public Health, computer science, biology, bioinformatics,
- Boston, MA
BRX mediates feedback between brassinosteroid levels and auxin signalling in root growth
Céline F. Mouchel1, Karen S. Osmont1 & Christian S. Hardtke1
- Department of Plant Molecular Biology, Biophore Building, University of Lausanne, CH-1015 Lausanne, Switzerland
Correspondence to: Christian S. Hardtke1 The microarray experiments have been deposited in the Array Express Database under accession numbers E-MEXP-635 and M-MEXP- 637. Correspondence and requests for materials should be addressed to C.S.H. (Email: christian.hardtke@unil.ch).
Abstract
Brassinosteroid and auxin decisively influence plant development, and overlapping transcriptional responses to these phytohormones suggest an interaction between the two pathways1, 2, 3. However, whether this reflects direct feedback or merely parallel inputs on common targets is unclear. Here we show that in Arabidopsis roots, this interaction is mediated by BREVIS RADIX (BRX), which is required for optimal root growth4. We demonstrate that the brx phenotype results from a root-specific deficiency of brassinosteroid and is due to reduced, BRX-dependent expression of a rate-limiting enzyme in brassinosteroid biosynthesis. Unexpectedly, this deficiency affects the root expression level of
15% of all Arabidopsis genes, but the transcriptome profile can be restored to wild type by brassinosteroid treatment. Thus, proper brassinosteroid levels are required for the correct expression of many more genes than previously suspected. Moreover, embryonic or post-embryonic brassinosteroid application fully or partially, respectively, rescues the brx phenotype. Further, auxin-responsive gene expression is globally impaired in brx, demonstrating that brassinosteroid levels are rate-limiting for auxin-responsive transcription. BRX expression is strongly induced by auxin and mildly repressed by brassinolide, which means that BRX acts at the nexus of a feedback loop that maintains threshold brassinosteroid levels to permit optimal auxin action.
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