An Arabidopsis mutant atcsr-2 exhibits high cadmium stress sensitivity involved in the restriction of H2S emission
An Arabidopsis mutant atcsr-2 exhibits high cadmium stress sensitivity involved in the restriction of H2S emission
复制标题
拟南芥突变体 atcsr-2 表现出与限制 H2S 排放有关的高镉胁迫敏感性
DOI：
10.1631/jzus.b1200089
复制
发表时间：
2012-12-01
影响因子：
5.1
通讯作者：
Pei, Yan-xi
中科院分区：
文献类型：
--
作者：
Li, Ya-wei;Gong, Ze-hua;Pei, Yan-xi
AtCSR基因编码多肽-脯氨基顺式/反式异构酶(PPIase)，该酶能加速蛋白质合成之前的肽键的顺式/反式异构化。在我们的研究中，我们发现AtCSR与拟南芥对镉(Cd)的敏感反应有关。我们的结果表明，在野生型拟南芥中，镉胁迫触发了AtCSR的表达。Cd~(2+)诱导了一些负责Cd~(2+)转运到液泡中的基因的表达，而与Cd~(2+)从环境中吸收相关的铁调节转运蛋白1(IRT1)的表达不被诱导。Cd转运相关基因的表达不受Cd胁迫的影响，而经Cd~(2+)处理的atcsr-2中IRT的表达显著增加。谷胱甘肽-1(GSH1)的表达与GSH的表达一致，但ATCSR-2在Cd~(2+)处理下的表达明显低于野生型。此外，丙二醛(MDA)、过氧化氢和镉的含量以及一些抗氧化酶的活性在野生型和atcsr-2之间存在差异。近年来，硫化氢(H_2S)已被确认为第三种气体发射器。结果表明，在野生型和atcsr-2中，H_2S释放相关基因和Cd诱导的螯合转运基因的表达模式匹配良好，H_2S可以调节Cd诱导基因的表达，减轻Cd的毒害作用。最后，提出了一个可能的建议：下调atcsr-2，依赖于H_2S气体递质，不仅削弱了Cd~(2+)的螯合作用，而且减少了Cd~(2+)向液泡的运输，促进了Cd~(2+)的同化，从而使atcsr-2突变体对Cd胁迫敏感。
The gene AtCSR encodes peptidyl-prolyl cis/trans isomerases (PPIases) that accelerate energetically unfavorable cis/trans isomerization of the peptide bond preceding proline production. In our studies, we found that AtCSR was associated with cadmium (Cd)-sensitive response in Arabidopsis. Our results show that AtCSR expression was triggered by Cd-stress in wild type Arabidopsis. The expression of some genes responsible for Cd2+ transportation into vacuoles was induced, and the expression of the iron-regulated transporter 1 (IRT1) related to Cd2+ absorption from the environment was not induced in wild type with Cd2+ treatment. The expression of Cd-transportation related genes was not in response to Cd-stress, whereas IRT expression increased dramatically in atcsr-2 with Cd2+ treatment. The expression of glutathione 1 (GSH1) was consistent with GSH being much lower in atcsr-2 in comparison with the wild type with Cd2+ treatment. Additionally, malondialdehyde (MDA), hydrogen peroxide, and Cd2+ contents, and activities of some antioxidative enzymes, differed between the wild type and atcsr-2. Hydrogen sulfide (H2S) has been confirmed as the third gas-transmitter over recent years. The findings revealed that the expression pattern of H2S-releasing related genes and that of Cd-induced chelation and transportation genes matched well in the wild type and atcsr-2, and H2S could regulate the expression of the Cd-induced genes and alleviate Cd-triggered toxicity. Finally, one possible suggestion was given: down-regulation of atcsr-2, depending on H2S gas-transmitter not only weakened Cd2+ chelation, but also reduced Cd2+ transportation into vacuoles, as well as enhancing the Cd2+ assimilation, thus rendering atcsr-2 mutant sensitive to Cd-stress.