A key general stress response motif is regulated non‐uniformly by CAMTA transcription factors. (19th August 2014)

• Record Type: Journal Article
• Authors: Benn, Geoffrey; Wang, Chang‐Quan; Hicks, Derrick R.; Stein, Jeffrey; Guthrie, Cade; Dehesh, Katayoon
• Is Part Of: Plant journal. Volume 80:Number 1(2014:Oct.)
• Page Start: 82
• Page End: 92
• Publication Date: 2014-08-19
• Subjects: Plant molecular biology -- Periodicals; Plant cells and tissues -- Periodicals; Botany -- Periodicals; 580
• DOI: 10.1111/tpj.12620
• Languages: English
• ISSNs: 0960-7412

Abstract

<abstract abstract-type="main" id="tpj12620-abs-0001"> <title>Summary</title> <p>Plants cope with environmental challenges by rapidly triggering and synchronizing mechanisms governing stress‐specific and general stress response (GSR) networks. The GSR acts rapidly and transiently in response to various stresses, but the underpinning mechanisms have remained elusive. To define GSR regulatory components we have exploited the <italic>Rapid Stress Response Element</italic> (<italic>RSRE</italic>), a previously established functional GSR motif, using Arabidopsis plants expressing a <italic>4xRSRE::Luciferase</italic> (<italic>RSRE::LUC</italic>) reporter. Initially, we searched public microarray datasets and found an enrichment of <italic>RSRE</italic> in promoter sequences of stress genes. Next, we treated <italic>RSRE::LUC</italic> plants with wounding and a range of rapidly stress‐inducible hormones and detected a robust LUC activity solely in response to wounding. Application of two Ca<sup>2+</sup> burst inducers, flagellin22 (flg22) and oligogalacturonic acid, activated <italic>RSRE</italic> strongly and systemically, while the Ca<sup>2+</sup> chelator ethylene glycol tetraacetic acid (EGTA) significantly reduced wound induction of <italic>RSRE::LUC</italic>. In line with the signaling function of Ca<sup>2+</sup> in transduction events leading to activation of <italic>RSRE</italic>, we examined the role of CALMODULIN‐BINDING TRANSCRIPTIONAL ACTIVATORs (CAMTAs) in <italic>RSRE</italic> induction. Transient expression assays displayed CAMTA3 induction of <italic>RSRE</italic> and not that of the mutated element <italic>mRSRE</italic>. Treatment of selected <italic>camta</italic> mutant lines integrated into <italic>RSRE::LUC</italic> parent plant, with wounding, flg22, and freezing, established a differential function of these CAMTAs in potentiating the activity of <italic>RSRE</italic>. Wound response studies using <italic>camta</italic> double mutants revealed a cooperative function of CAMTAs2 and 4 with CAMTA 3 in the <italic>RSRE</italic> regulation. These studies provide insights into governing components of transduction events and reveal transcriptional modules that tune the expression of a key GSR motif.</p> </abstract>