Biotechnology Research Institute, Chinese Academy of Agricultural Sciences, Beijing 100081, China.
Plant Physiol. 2011 Oct;157(2):854-65. doi: 10.1104/pp.111.179028. Epub 2011 Aug 10.
Accumulating investigations reveal that ethylene signaling is involved in the salt response in Arabidopsis (Arabidopsis thaliana), and it has been reported that overexpression of a number of ethylene response factor (ERF) genes enhances salt tolerance; however, transcriptional regulation of the ethylene signal component ETHYLENE INSENSITIVE3 (EIN3) in the salt response has not been clearly defined. Consulting microarray data and transcriptional confirmations showed that three of the ERF genes were ethylene and salt inducible, named ESE1 to ESE3. Additionally, the expression of one of the ESE genes (ESE1) was suppressed in ein2, ein3-1, eil1-3, and ein3 eil1 but enhanced in EIN3-overexpressing (EIN3ox) lines. Inhibitors of ethylene biosynthesis, aminoethoxyvinylglycine, and ethylene action, AgNO₃, reduced the expression of ESE1, while ethylene overproduction eto mutants enhanced the expression of ESE1, indicating that ESE1 is an ethylene-modulated gene downstream of EIN3/EIL1. Further analyses with biochemical and molecular approaches revealed that EIN3 physically binds to the ESE1 promoter, demonstrating that ESE1 was one target of EIN3. ESE1 in turn binds to promoters of salt-related genes, such as RD29A and COR15A. Moreover, either EIN3ox or ESE1ox was sufficient to enhance transcript levels of salt-related genes and salt tolerance. In addition, ESE1ox in ein3 enhanced the salt response during seed germination and seedling development, demonstrating that ESE1 is genetically downstream of EIN3. Thus, the evidence in this report reveals that the transcriptional complex of EIN3-ESE1 is a crucial event in the salt response, thereby connecting the transcriptional regulation of EIN3 and the downstream ERF protein ESE1 in the salt response.
越来越多的研究表明乙烯信号参与了拟南芥的盐响应，并且已经报道过许多乙烯反应因子（ERF）基因的过表达增强了盐耐受性；然而，乙烯信号组分 ETHYLENE INSENSITIVE3（EIN3）在盐响应中的转录调控还没有明确界定。参考微阵列数据和转录验证表明，三个 ERF 基因是乙烯和盐诱导的，分别命名为 ESE1 到 ESE3。此外，其中一个 ESE 基因（ESE1）的表达在 ein2、ein3-1、eil1-3 和 ein3 eil1 中受到抑制，但在 EIN3 过表达（EIN3ox）系中增强。乙烯生物合成抑制剂氨基乙氧基乙烯基甘氨酸和乙烯作用抑制剂 AgNO₃降低了 ESE1 的表达，而乙烯过产生物 eto 突变体增强了 ESE1 的表达，表明 ESE1 是 EIN3/EIL1 下游的一个乙烯调节基因。通过生化和分子方法的进一步分析表明，EIN3 物理结合到 ESE1 启动子上，表明 ESE1 是 EIN3 的一个靶标。ESE1 反过来又与盐相关基因（如 RD29A 和 COR15A）的启动子结合。此外，EIN3ox 或 ESE1ox 都足以增强盐相关基因和盐耐受性的转录水平。此外，ein3 中的 ESE1ox 增强了种子萌发和幼苗发育过程中的盐响应，表明 ESE1 在遗传上是 EIN3 的下游。因此，本报告中的证据表明，EIN3-ESE1 转录复合物是盐响应中的一个关键事件，从而将 EIN3 的转录调控与盐响应中的下游 ERF 蛋白 ESE1 联系起来。
