Abscisic acid induces CBF gene transcription and subsequent induction of cold-regulated genes via the CRT promoter element

• Published in: Plant physiology (Bethesda) Vol. 135; no. 3; pp. 1710 - 1717
• Main Authors: Knight, H, Zarka, D.G, Okamoto, H, Thomashow, M.F, Knight, M.R
• Format: Journal Article
• Language: English
• Published: Rockville, MD American Society of Plant Biologists 01.07.2004; American Society of Plant Physiologists
• Subjects: abscisic acid; Abscisic Acid - pharmacology; Arabidopsis; Arabidopsis - genetics; Arabidopsis Proteins - genetics; Base Sequence; Biological and medical sciences; c-repeat binding factor; cold stress; Cold Temperature; dehydration-responsive element binding protein; Desiccation; DNA Primers; DNA, Plant - genetics; Drought; Environmental Stress and Adaptation; Ethanol; Fundamental and applied biological sciences. Psychology; Gene expression; Gene Expression Regulation, Plant - drug effects; Gene induction; Genes; Low temperature; Molecular and cellular biology; Molecular genetics; molecular sequence data; nucleotide sequences; Plant cells; plant proteins; Promoter regions; Promoter Regions, Genetic - drug effects; Promoter Regions, Genetic - genetics; protein synthesis; Proteins; Seedlings; transcription (genetics); transcription factors; Transcription, Genetic - drug effects; Transcriptional Activation; Arabidopsis thaliana; Signal transduction; Gene; Cruciferae; Dicotyledones; Angiospermae; Abscisic acid; Spermatophyta; Biological accumulation; Gene expression; Low temperature
• ISSN: 0032-0889; 1532-2548
• DOI: 10.1104/pp.104.043562

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.