TGA Transcription Factors Activate the Salicylic Acid-Suppressible Branch of the Ethylene-Induced Defense Program by Regulating ORA59 Expression1[C][W]
TGA Transcription Factors Activate the Salicylic Acid-Suppressible Branch of the Ethylene-Induced Defense Program by Regulating ORA59 Expression1[C][W]
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DOI：
10.1104/pp.114.243360
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发表时间：
2014-07
期刊：
影响因子：
7.4
通讯作者：
Mark Zander;Corinna Thurow;C. Gatz
中科院分区：
文献类型：
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作者：
Mark Zander;Corinna Thurow;C. Gatz
两个拮抗激素途径在其中一个途径的关键激活剂的启动子处合并。水杨酸（SA）是一种防御活体营养型病原体所必需的激素，通过抑制茉莉酸-乙烯（ET）防御反应来触发植物对坏死型攻击者的敏感性增加。在这里，我们表明，这种疾病促进SA的效果是废除在植物缺乏三个相关的TGACG序列特异性结合蛋白TGA 2，TGA 5和TGA 6（II类TGA）。用ET前体1-氨基环丙烷-1-羧酸（ACC）处理植物后，所有那些被SA抑制的基因的激活依赖于II类TGA。而不是TGA结合位点，GCC盒基序显着富集在相应的启动子。GCC-盒基序被APETALA 2/乙烯应答因子（ERF）超家族成员识别。在11个激活ACC诱导的APETALA 2/ERF中，SA仅强烈抑制ORA 59（八癸烷类反应性拟南芥APETALA 2/乙烯反应因子结构域蛋白59）和ERF 96。ORA 59是茉莉酸-ET-诱导的防御程序的主要调节剂。在tga 2 tga 5 tga 6三重突变体中，ORA 59转录物水平未达到最大水平，并且该残余活性不能被SA抑制。ORA 59启动子含有一个必需的TGA结合位点，是II类TGA的直接靶点，如染色质免疫沉淀实验所示。我们认为，II类TGAs在ORA 59启动子构成一个重要的调控枢纽，激活和SA抑制ACC诱导的基因。
Two antagonistic hormonal pathways merge at the promoter of a crucial activator of one of the pathways. Salicylic acid (SA), a hormone essential for defense against biotrophic pathogens, triggers increased susceptibility of plants against necrotrophic attackers by suppressing the jasmonic acid-ethylene (ET) defense response. Here, we show that this disease-promoting SA effect is abolished in plants lacking the three related TGACG sequence-specific binding proteins TGA2, TGA5, and TGA6 (class II TGAs). After treatment of plants with the ET precursor 1-aminocyclopropane-1-carboxylic acid (ACC), activation of all those genes that are suppressed by SA depended on class II TGAs. Rather than TGA binding sites, GCC-box motifs were significantly enriched in the corresponding promoters. GCC-box motifs are recognized by members of the superfamily of APETALA2/ETHYLENE RESPONSE FACTORs (ERFs). Of 11 activating ACC-induced APETALA2/ERFs, only ORA59 (for OCTADECANOID-RESPONSIVE ARABIDOPSIS APETALA2/ETHYLENE RESPONSE FACTOR domain protein59) and ERF96 were strongly suppressed by SA. ORA59 is the master regulator of the jasmonic acid-ET-induced defense program. ORA59 transcript levels do not reach maximal levels in the tga2 tga5 tga6 triple mutant, and this residual activity cannot be suppressed by SA. The ORA59 promoter contains an essential TGA binding site and is a direct target of class II TGAs as revealed by chromatin immunoprecipitation experiments. We suggest that class II TGAs at the ORA59 promoter constitute an important regulatory hub for the activation and SA suppression of ACC-induced genes.