Letter
Nature 451, 480-484 (24 January 2008) | doi:10.1038/nature06520; Received 28 September 2007; Accepted 28 November 2007
A molecular framework for light and gibberellin control of cell elongation
Miguel de Lucas1,4, Jean-Michel Davière1,4, Mariana Rodríguez-Falcón1,4, Mariela Pontin1, Juan Manuel Iglesias-Pedraz1, Séverine Lorrain2, Christian Fankhauser2, Miguel Angel Blázquez3, Elena Titarenko1 & Salomé Prat1
- Departamento de Genética Molecular de Plantas, Centro Nacional de Biotecnología-CSIC, Campus Univ. Autónoma de Madrid, Cantoblanco. c/ Darwin 3, 28049 Madrid, Spain
- Centre for Integrative Genomics, University of Lausanne, Genopode Building, CH-1015 Lausanne, Switzerland
- Instituto de Biología Molecular y Celular de Plantas, Universidad Politécnica de Valencia, Consejo Superior de Investigaciones Científicas, 46022 Valencia, Spain
- These authors contributed equally to this work.
Correspondence to: Salomé Prat1 Correspondence and requests for materials should be addressed to S.P. (Email: sprat@cnb.uam.es).
Cell elongation during seedling development is antagonistically regulated by light and gibberellins (GAs)1, 2. Light induces photomorphogenesis, leading to inhibition of hypocotyl growth, whereas GAs promote etiolated growth, characterized by increased hypocotyl elongation. The mechanism underlying this antagonistic interaction remains unclear. Here we report on the central role of the Arabidopsis thaliana nuclear transcription factor PIF4 (encoded by PHYTOCHROME INTERACTING FACTOR 4)3 in the positive control of genes mediating cell elongation and show that this factor is negatively regulated by the light photoreceptor phyB (ref. 4) and by DELLA proteins that have a key repressor function in GA signalling5. Our results demonstrate that PIF4 is destabilized by phyB in the light and that DELLAs block PIF4 transcriptional activity by binding the DNA-recognition domain of this factor. We show that GAs abrogate such repression by promoting DELLA destabilization, and therefore cause a concomitant accumulation of free PIF4 in the nucleus. Consistent with this model, intermediate hypocotyl lengths were observed in transgenic plants over-accumulating both DELLAs and PIF4. Destabilization of this factor by phyB, together with its inactivation by DELLAs, constitutes a protein interaction framework that explains how plants integrate both light and GA signals to optimize growth and development in response to changing environments.
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