Zinc-Finger Transcription Factor ZAT6 Positively Regulates Cadmium Tolerance through the Glutathione-Dependent Pathway in Arabidopsis
Zinc-Finger Transcription Factor ZAT6 Positively Regulates Cadmium Tolerance through the Glutathione-Dependent Pathway in Arabidopsis
复制标题
锌指转录因子 ZAT6 通过谷胱甘肽依赖性途径正向调节拟南芥的镉耐受性
DOI：
10.1104/pp.15.01882
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发表时间：
2016-05-01
期刊：
影响因子：
7.4
通讯作者：
Cao, Shuqing
中科院分区：
文献类型：
--
作者：
Chen, Jian;Yang, Libo;Cao, Shuqing
镉（Cd）是一种对动植物具有高毒性的环境污染物。谷胱甘肽（GSH）依赖的植物螯合素（PC）合成途径是植物积累和耐受镉的重要机制之一。然而，参与调节GSH依赖的PC合成途径的转录因子仍然在很大程度上未知。在这里，我们确定了一个拟南芥（拟南芥）镉抗性突变体xcd 2-D（XVE系统诱导的镉耐受2）使用正向遗传学方法。xcd 2-D突变的突变基因编码一种已知的锌指转录因子ZAT 6。过量表达ZAT 6的转基因植株对Cd的耐受性显著提高，而ZAT 6功能的丧失则导致其对Cd的耐受性下降。增加镉积累和耐受性在ZAT 6过表达系GSH依赖和相关的镉激活PC的合成，这是与协调激活PC合成相关的基因表达。相反，ZAT 6功能的丧失降低了镉的积累和耐受性，这是伴随着PC合成和基因表达的废除。进一步分析表明，ZAT 6正调控GSH 1、GSH 2、PCS 1和PCS 2的转录，但ZAT 6能够在体内特异性结合GSH 1启动子。一致地，GSH 1的过表达已被证明可以恢复zat 6 -1突变体中的Cd敏感性，这表明GSH 1是ZAT 6的关键靶标。综上所述，我们的数据提供的证据表明，ZAT 6协调激活PC合成相关的基因表达，并直接靶向GSH 1正向调节镉的积累和耐性在拟南芥。
Cadmium (Cd) is an environmental pollutant with high toxicity to animals and plants. It has been established that the glutathione (GSH)-dependent phytochelatin (PC) synthesis pathway is one of the most important mechanisms contributing to Cd accumulation and tolerance in plants. However, the transcription factors involved in regulating GSH-dependent PC synthesis pathway remain largely unknown. Here, we identified an Arabidopsis (Arabidopsis thaliana) Cd-resistant mutant xcd2-D (XVE system-induced cadmium-tolerance2) using a forward genetics approach. The mutant gene underlying xcd2-D mutation was revealed to encode a known zinc-finger transcription factor, ZAT6. Transgenic plants overexpressing ZAT6 showed significant increase of Cd tolerance, whereas loss of function of ZAT6 led to decreased Cd tolerance. Increased Cd accumulation and tolerance in ZAT6-overexpressing lines was GSH dependent and associated with Cd-activated synthesis of PC, which was correlated with coordinated activation of PC-synthesis related gene expression. By contrast, loss of function of ZAT6 reduced Cd accumulation and tolerance, which was accompanied by abolished PC synthesis and gene expression. Further analysis revealed that ZAT6 positively regulates the transcription of GSH1, GSH2, PCS1, and PCS2, but ZAT6 is capable of specifically binding to GSH1 promoter in vivo. Consistently, overexpression of GSH1 has been shown to restore Cd sensitivity in the zat6-1 mutant, suggesting that GSH1 is a key target of ZAT6. Taken together, our data provide evidence that ZAT6 coordinately activates PC synthesis-related gene expression and directly targets GSH1 to positively regulate Cd accumulation and tolerance in Arabidopsis.