Your browser version may not work well with NCBI's Web applications. More information here...
1: Plant Cell. 2008 Aug;20(8):2117-29. Epub 2008 Aug 29.
Related Articles, Links
Click here to read Click here to read
The cold-inducible CBF1 factor-dependent signaling pathway modulates the accumulation of the growth-repressing DELLA proteins via its effect on gibberellin metabolism.

Achard P, Gong F, Cheminant S, Alioua M, Hedden P, Genschik P.

Institut de Biologie Moléculaire des Plantes, Centre National de la Recherche Scientifique, Unité Propre de Recherche 2357, Conventioné avec l'Université Louis Pasteur, 67084 Strasbourg, France.

Plants have evolved robust mechanisms to respond and adapt to unfavorable environmental conditions, such as low temperature. The C-repeat/drought-responsive element binding factor CBF1/DREB1b gene encodes a transcriptional activator transiently induced by cold that controls the expression of a set of genes responding to low temperature (the CBF regulon). Constitutive expression of CBF1 confers freezing tolerance but also slows growth. Here, we propose that low temperature-induced CBF1 expression restrains growth at least in part by allowing the accumulation of DELLAs, a family of nuclear growth-repressing proteins, the degradation of which is stimulated by gibberellin (GA). We show that cold/CBF1 enhances the accumulation of a green fluorescent protein (GFP)-tagged DELLA protein (GFP-RGA) by reducing GA content through stimulating expression of GA-inactivating GA 2-oxidase genes. Accordingly, transgenic plants that constitutively express CBF1 accumulate less bioactive GA and as a consequence exhibit dwarfism and late flowering. Both phenotypes are suppressed when CBF1 is expressed in a line lacking two DELLA proteins, GA-INSENSITIVE and REPRESSOR OF GA1-3. In addition, we show that DELLAs contribute significantly to CBF1-induced cold acclimation and freezing tolerance by a mechanism that is distinct from the CBF regulon. We conclude that DELLAs are components of the CBF1-mediated cold stress response.

Publication Types:
PMID: 18757556 [PubMed - in process]

PMCID: PMC2553604 [Available on 08/01/09]