Plant Physiology Preview
Published on July 9, 2004; 10.1104/pp.104.043562
Received March 26, 2004
Returned for revision April 30, 2004
Accepted April 30, 2004
Abscisic Acid Induces CBF Gene Transcription and Subsequent Induction of Cold-Regulated Genes via the CRT Promoter Element
Heather Knight *, Daniel G. Zarka , Haruko Okamoto , Michael F. Thomashow , and Marc R. Knight
Department of Plant Sciences, University of Oxford, Oxford, OX1 3RB, United Kingdom
Department of Energy Plant Research Laboratory
Department of Energy Plant Research Laboratory and Department of Crop and Soil Sciences, Michigan State University, East Lansing, Michigan 48824
* Corresponding author; email: heather.knight{at}plants.ox.ac.uk.
Many cold-regulated genes of Arabidopsis are inducible by abscisic acid (ABA) as well as by cold. This has been thought to occur via two separate signaling pathways, with ABA acting via ABA-responsive promoter elements and low temperature activating the C-repeat element (CRT; dehydration-responsive) promoter element via CBF (DREB1) transcription factors. We show here that ABA is also capable of activating the CRT promoter element. Although the more recently discovered ABA-inducible CBF4 transcription factor might have accounted for this, we show here that CBF1-3 transcript levels also increase in response to elevated ABA levels. This increase in CBF1-3 transcript levels appears to be at least in part due to increased activity of the CBF promoters in response to ABA. A total of 125 bp of the CBF2 promoter, which has previously been shown to be sufficient for cold-, mechanical-, and cycloheximide-induced expression, was also sufficient for ABA-induced expression. However, the ABA-responsive promoter element-like motif within this region is not needed for ABA-induced expression. An observed increase in CBF protein levels after ABA treatment, together with previous data showing that increased CBF levels are sufficient for cold-regulated gene induction, suggests that ABA-induced increases in CBF1-3 transcript levels do have the potential to activate the CRT. Our data indicate therefore that activation of the CRT may also occur via a novel ABA-inducible signaling pathway using the normally cold-inducible CBFs.
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