The PSE1 gene modulates lead tolerance in Arabidopsis

The PSE1 gene modulates lead tolerance in Arabidopsis
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PSE1 基因调节拟南芥的铅耐受性

DOI:
10.1093/jxb/erw251
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发表时间:
2016-08-01
影响因子:
6.9
通讯作者:
Cao, Shuqing
Cao, Shuqing
中科院分区:
生物学1区
文献类型:
--
作者:
Fan, Tingting;Yang, Libo;Cao, Shuqing

文献摘要

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PSE 1主要通过激活植物螯合素合成相关基因的表达,并至少部分通过激活PDR 12的表达来调节植物对铅的耐受性。铅(Pb)是一种对植物具有高度毒性的重金属污染物。然而,植物耐铅性的调控机制知之甚少。在这里,我们表明,PSE 1基因赋予拟南芥铅耐受性。通过筛选T-DNA插入突变体,获得了一株新的铅敏感突变体pse 1 -1(Pb-sensitive 1)。PSE 1编码一个未知的蛋白质,具有NC结构域,定位于细胞质中。铅胁迫诱导了PSE 1的表达,pse 1 -1功能缺失突变体表现出对铅的敏感性增强,过量表达PSE 1可提高其对铅的耐受性。PSE 1过表达的植物表现出增加铅的积累,这是伴随着植物螯合素(PC)的合成和相关基因的表达激活。与此相反,pse 1 -1突变体表现出减少铅积累,这是与PC合成和相关基因表达下降。此外,在遭受Pb胁迫的PSE 1过表达植物中,PDR 12的表达也增加。我们的研究结果表明,PSE 1调节铅的耐受性主要通过谷胱甘肽依赖的PC合成激活参与PC合成的基因的表达,至少部分通过激活ABC转运蛋白PDR 12/ABCG 40的表达。
PSE1 regulates Pb tolerance mainly through GSH-dependent phytochelatin synthesis by activating the expression of the genes involved in phytochelatin synthesis and at least partially through activating the expression of PDR12.Lead (Pb) is a dangerous heavy metal contaminant with high toxicity to plants. However, the regulatory mechanism of plant Pb tolerance is poorly understood. Here, we showed that the PSE1 gene confers Pb tolerance in Arabidopsis. A novel Pb-sensitive mutant pse1-1 (Pb-sensitive1) was isolated by screening T-DNA insertion mutants. PSE1 encodes an unknown protein with an NC domain and was localized in the cytoplasm. PSE1 was induced by Pb stress, and the pse1-1 loss-of-function mutant showed enhanced Pb sensitivity; overexpression of PSE1 resulted in increased Pb tolerance. PSE1-overexpressing plants showed increased Pb accumulation, which was accompanied by the activation of phytochelatin (PC) synthesis and related gene expression. In contrast, the pse1-1 mutant showed reduced Pb accumulation, which was associated with decreased PC synthesis and related gene expression. In addition, the expression of PDR12 was also increased in PSE1-overexpressing plants subjected to Pb stress. Our results suggest that PSE1 regulates Pb tolerance mainly through glutathione-dependent PC synthesis by activating the expression of the genes involved in PC synthesis and at least partially through activating the expression of the ABC transporter PDR12/ABCG40.