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首页> 外文期刊>Plant physiology >Characterization of AtALMT1 Expression in Aluminum-Inducible Malate Release and Its Role for Rhizotoxic Stress Tolerance in Arabidopsis
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Characterization of AtALMT1 Expression in Aluminum-Inducible Malate Release and Its Role for Rhizotoxic Stress Tolerance in Arabidopsis

机译:铝诱导苹果酸释放中AtALMT1表达的表征及其在拟南芥中的根瘤菌抗逆性的作用

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Malate transporters play a critical role in aluminum (Al) tolerance responses for some plant species, such as Arabidopsis (Arabidopsis thaliana). Here, we further characterize AtALMT1, an Arabidopsis aluminum-activated malate transporter, to clarify its specific role in malate release and Al stress responses. Malate excretion from the roots of accession Columbia was sharply induced by Al, which is concomitant with the induction of AtALMT1 gene expression. The malate release was specific for Al among rhizotoxic stressors, namely cadmium, copper, erbium, lanthanum, sodium, and low pH, which accounts for the specific sensitivity of a null mutant to Al stress. Al-specific malate excretion can be explained by a combined regulation of AtALMT1 expression and activation of AtALMT1 protein, which is specific for Al. Although low pH treatment slightly induced gene expression, other treatments did not. In addition, malate excretion in Al-activated seedlings was rapidly stopped by removing Al from the solution. Other rhizotoxic stressors were not effective in maintaining malate release. Protein kinase and phosphatase inhibitor studies indicated that reversible phosphorylation was important for the transcriptional and posttranslational regulation of AtALMT1. AtALMT1 promoter-o-glucuronidase fusion lines revealed that AtALMT1 has restricted expression within the root, such that unnecessary carbon loss is likely minimized. Lastly, a natural nonsense mutation allele of AtALMT1 was identified from the Al-hypersensitive natural accession Warschau-1.
机译:苹果酸转运蛋白在某些植物物种(如拟南芥(Arabidopsis thaliana))对铝(Al)的耐受性响应中起着至关重要的作用。在这里,我们进一步表征拟南芥铝激活苹果酸转运蛋白AtALMT1,以阐明其在苹果酸释放和铝胁迫响应中的特定作用。 Al可以强烈地诱导从登录哥伦比亚的根部排出苹果酸,这与AtALMT1基因表达的诱导同时发生。苹果酸的释放对铝的根际毒性应激源(镉,铜,,镧,钠和低pH)具有特异性,这说明了无效突变体对Al胁迫的特异性敏感性。 Al特有的苹果酸排泄可以通过AtALMT1表达和AtALMT1蛋白(对Al特异)的激活的联合调节来解释。尽管低pH处理略微诱导了基因表达,但其他处理却没有。此外,通过从溶液中去除铝,可以迅速停止铝活化幼苗中的苹果酸排泄。其他根瘤菌应激源不能有效维持苹果酸的释放。蛋白激酶和磷酸酶抑制剂的研究表明,可逆的磷酸化对于AtALMT1的转录和翻译后调控非常重要。 AtALMT1启动子-o-葡糖醛酸糖苷酶融合细胞系显示AtALMT1在根内表达受到限制,因此不必要的碳损失可能会降至最低。最后,从Al超敏感天然登录号Warschau-1中鉴定出AtALMT1的天然无义突变等位基因。

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