Cold treatment enhances lead resistance in Arabidopsis
Cold treatment enhances lead resistance in Arabidopsis
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冷处理增强拟南芥的铅抗性
DOI：
10.1007/s11738-009-0369-1
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发表时间：
2010-01-01
影响因子：
2.6
通讯作者：
Sun, Zehua
中科院分区：
文献类型：
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作者：
Cao, Shuqing;Bian, Xiaohui;Sun, Zehua
作为固着生物，植物通常同时经历几种逆境。结果表明，胁迫交叉耐受性可由不同的胁迫因子诱导，包括生物因子以及重金属、低氧、紫外线-B辐射、高温、高盐、干旱和低温胁迫。然而，目前还不清楚拟南芥是否对冷和铅（Pb）胁迫存在交叉耐受性。在这项研究中，我们表明，冷预处理增强了拟南芥的抗Pb（II），所示的根长，鲜重，叶绿素含量在冷处理的植物比对照降低。在低温处理的幼苗，较低的铅含量检测到根和地上部相比，对照。这至少部分与AtPDR 12基因表达的激活有关，AtPDR 12基因是一种将Pb（II）和/或含Pb（II）的有毒化合物从细胞质排除到细胞外部的泵。这一发现进一步支持的遗传证据表明，冷处理是无法提高atpdr 12突变体的抗Pb（II）胁迫，但可以提高铅（II）抗性的野生型。此外，我们还发现，冷诱导的增强Pb（II）抗性是谷胱甘肽无关的。综上所述，所有这些结果表明，低温处理增强了拟南芥的Pb（II）抗性，至少部分，通过激活AtPDR 12基因的表达。
As sessile organisms, plants usually experience several stresses simultaneously. It was shown that stress cross-tolerance may be induced by different stressors, including biotic factors as well as heavy metal, hypoxia, ultraviolet-B radiation, heat, high salt, drought, and cold stresses. However, it is unclear whether there is a cross-tolerance toward cold and lead (Pb) stresses in Arabidopsis. In this study, we showed that cold pretreatment enhanced Pb(II) resistance in Arabidopsis, as indicated by lower reduction of root length, fresh weight, and chlorophyll content in the cold-treated plants than the control ones. In the cold-treated seedlings, lower Pb contents were detected in roots and shoots in comparison to the control. This was associated, at least in part, with the activation of the expression of AtPDR12 gene, a pump excluding Pb(II) and/or Pb(II)-containing toxic compounds from the cytoplasm to the exterior of the cell. This finding was further supported by genetic evidence showing that cold treatment was unable to enhance resistance of atpdr12 mutant to Pb(II) stress but could enhance Pb(II) resistance of the wild type. In addition, we also found that cold-induced enhanced Pb(II) resistance was glutathione-independent. Taken together, all these results suggest that cold treatment enhanced Pb(II) resistance in Arabidopsis, at least in part, by activating the expression of AtPDR12 gene.