A key general stress response motif is regulated non-uniformly by CAMTA transcription factors.

A key general stress response motif is regulated non-uniformly by CAMTA transcription factors.
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DOI:
10.1111/tpj.12620
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发表时间:
2014-10
期刊:
The Plant journal : for cell and molecular biology
影响因子:
--
通讯作者:
Dehesh K
Dehesh K
中科院分区:
其他
文献类型:
--
作者:
Benn G;Wang CQ;Hicks DR;Stein J;Guthrie C;Dehesh K

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植物通过快速触发和同步控制胁迫特异性和一般胁迫反应(GSR)网络的机制科普环境挑战。GSR对各种压力的反应迅速而短暂,但其基础机制仍然难以捉摸。为了定义GSR调控元件,我们利用了快速应激反应元件(RSRE),一种先前建立的功能性GSR基序,使用表达4xRSRE::荧光素酶(RSRE::LUC)报告基因的拟南芥植物。最初,我们搜索了公共微阵列数据集,发现了应激基因启动子序列中RSRE的富集。接下来,我们用创伤和一系列快速应激诱导激素处理RSRE::LUC植物,并检测到仅响应于创伤的鲁棒LUC活性。应用两种Ca2+爆发诱导剂,鞭毛蛋白22(flg22)和寡聚半乳糖醛酸,激活RSRE强烈和全身,而Ca2+螯合剂EGTA显着降低RSRE::LUC的伤口诱导。根据Ca 2+在导致RSRE激活的转导事件中的信号传导功能,我们研究了钙调蛋白结合转录激活因子(CAMTA)在RSRE诱导中的作用。瞬时表达测定显示CAMTA 3诱导RSRE,而不是突变元件mRSRE。用创伤、flg 22和冷冻处理整合到RSRE::LUC亲本植物中的所选CAMTA突变株系,建立了这些CAMTA在增强RSRE活性中的差异功能。使用camta双突变体的伤口反应研究揭示了CAMTA 2和4与CAMTA 3在RSRE调节中的协同功能。这些研究提供了深入了解转导事件的管理组件,并揭示了转录模块,调整一个关键的GSR基序的表达。
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 Rapid Stress Response Element (RSRE), a previously established functional GSR motif, using Arabidopsis plants expressing a 4xRSRE::Luciferase (RSRE::LUC) reporter. Initially, we searched public microarray datasets and found an enrichment of RSRE in promoter sequences of stress genes. Next, we treated RSRE::LUC 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 Ca2+ burst inducers, flagellin22 (flg22) and oligogalacturonic acid, activated RSRE strongly and systemically, while the Ca2+ chelator EGTA significantly reduced wound induction of RSRE::LUC. In line with the signaling function of Ca2+ in transduction events leading to activation of RSRE, we examined role of CALMODULIN-BINDING TRANSCRIPTIONAL ACTIVATORs (CAMTAs) in RSRE induction. Transient expression assays displayed CAMTA3 induction of RSRE and not that of the mutated element mRSRE. Treatment of selected camta mutant lines integrated into RSRE::LUC parent plant, with wounding, flg22, and freezing, established a differential function of these CAMTAs in potentiating the activity of RSRE. Wound response studies using camta double mutants revealed cooperative function of CAMTAs2 and 4 with CAMTA 3 in the RSRE regulation. These studies provide insight into governing components of transduction events and reveal transcriptional modules that tune expression of a key GSR motif.
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