首页> 美国卫生研究院文献>Plant Physiology >Major Alterations of the Regulation of Root NO3− Uptake Are Associated with the Mutation of Nrt2.1 and Nrt2.2 Genes in Arabidopsis
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Major Alterations of the Regulation of Root NO3− Uptake Are Associated with the Mutation of Nrt2.1 and Nrt2.2 Genes in Arabidopsis

机译:根规的重大变更 NO3-的摄取与突变有关 Nrt2.1和Nrt2.2基因的克隆 拟南芥

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摘要

The role of AtNrt2.1 and AtNrt2.2 genes, encoding putative NO3 transporters in Arabidopsis, in the regulation of high-affinity NO3 uptake has been investigated in the atnrt2 mutant, where these two genes are deleted. Our initial analysis of the atnrt2 mutant (S. Filleur, M.F. Dorbe, M. Cerezo, M. Orsel, F. Granier, A. Gojon, F. Daniel-Vedele [2001] FEBS Lett 489: 220–224) demonstrated that root NO3 uptake is affected in this mutant due to the alteration of the high-affinity transport system (HATS), but not of the low-affinity transport system. In the present work, we show that the residual HATS activity in atnrt2 plants is not inducible by NO3, indicating that the mutant is more specifically impaired in the inducible component of the HATS. Thus, high-affinity NO3 uptake in this genotype is likely to be due to the constitutive HATS. Root 15NO3 influx in the atnrt2 mutant is no more derepressed by nitrogen starvation or decrease in the external NO3 availability. Moreover, the mutant also lacks the usual compensatory up-regulation of NO3 uptake in NO3-fed roots, in response to nitrogen deprivation of another portion of the root system. Finally, exogenous supply of NH4+ in the nutrient solution fails to inhibit 15NO3 influx in the mutant, whereas it strongly decreases that in the wild type. This is not explained by a reduced activity of NH4+ uptake systems in the mutant. These results collectively indicate that AtNrt2.1 and/or AtNrt2.2 genes play a key role in the regulation of the high-affinity NO3 uptake, and in the adaptative responses of the plant to both spatial and temporal changes in nitrogen availability in the environment.
机译:已经在atnrt2中研究了编码拟南芥中假定的NO3 -转运蛋白的AtNrt2.1和AtNrt2.2基因在调节高亲和性NO3 -吸收中的作用。突变体,其中删除了这两个基因。我们对atnrt2突变体的初步分析(S. Filleur,MF Dorbe,M。Cerezo,M。Orsel,F。Granier,A。Gojon,F。Daniel-Vedele [2001] FEBS Lett 489:220–224)证明了该根由于高亲和力转运系统(HATS)的改变,NO3 -的吸收在此突变体中受到影响,而低亲和力转运系统的改变则不受此影响。在目前的工作中,我们表明atnrt2植物中的残留HATS活性不能被NO3 -诱导,这表明该突变体在HATS的可诱导成分中受到了更特别的损害。因此,该基因型中高亲和力的NO3 -摄取可能是由于组成型HATS引起的。根 15 NO3 -流入 atnrt2突变体不再被氮抑制 饥饿或减少外部NO3 - 可用性。而且,突变体也缺乏通常的补偿性 体内NO3 -吸收的上调 NO3 -根系对氮的响应 剥夺了根系统的另一部分。最后,外生的 营养液中NH4 + 的供应失败 抑制 15 NO3 -流入 突变体,而它大大降低了野生型的突变体。这是 NH4 + 活性降低无法解释 突变体中的摄取系统。这些结果共同表明 AtNrt2.1和/或AtNrt2.2基因起关键作用 在高亲和力调节中的作用 NO3 -的吸收以及适应性反应 植物对氮的时空变化的影响 环境中的可用性。

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