Cerezo M, Tillard P, Filleur S, Muños S, Daniel-Vedele F, Gojon A
Biochimie et Physiologie Moléculaire des Plantes, Unité Mixte de Recherche 5004, Agro-Montpellier/Centre National de la Recherche Scientifique/Institut National de la Recherche Agronomique/Université Montpellier 2, 34060 Montpellier cedex, France.
Plant Physiol. 2001 Sep;127(1):262-71. doi: 10.1104/pp.127.1.262.
The role of AtNrt2.1 and AtNrt2.2 genes, encoding putative NO(3)(-) transporters in Arabidopsis, in the regulation of high-affinity NO(3)(-) 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 NO(3)(-) 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 NO(3)(-), indicating that the mutant is more specifically impaired in the inducible component of the HATS. Thus, high-affinity NO(3)(-) uptake in this genotype is likely to be due to the constitutive HATS. Root (15)NO(3)(-) influx in the atnrt2 mutant is no more derepressed by nitrogen starvation or decrease in the external NO(3)(-) availability. Moreover, the mutant also lacks the usual compensatory up-regulation of NO(3)(-) uptake in NO(3)(-)-fed roots, in response to nitrogen deprivation of another portion of the root system. Finally, exogenous supply of NH(4)(+) in the nutrient solution fails to inhibit (15)NO(3)(-) influx in the mutant, whereas it strongly decreases that in the wild type. This is not explained by a reduced activity of NH(4)(+) 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 NO(3)(-) uptake, and in the adaptative responses of the plant to both spatial and temporal changes in nitrogen availability in the environment.
拟南芥中编码假定硝酸盐转运蛋白的AtNrt2.1和AtNrt2.2基因在高亲和力硝酸盐吸收调控中的作用，已在atnrt2突变体中进行了研究，该突变体中这两个基因已缺失。我们对atnrt2突变体（S. Filleur、M.F. Dorbe、M. Cerezo、M. Orsel、F. Granier、A. Gojon、F. Daniel-Vedele [2001] FEBS Lett 489: 220 - 224）的初步分析表明，由于高亲和力转运系统（HATS）的改变，该突变体的根系硝酸盐吸收受到影响，但低亲和力转运系统未受影响。在本研究中，我们表明atnrt2植株中残留的HATS活性不能被硝酸盐诱导，这表明该突变体在HATS的可诱导成分中存在更特异性的缺陷。因此，该基因型中的高亲和力硝酸盐吸收可能归因于组成型HATS。atnrt2突变体根系的（15）硝酸盐流入不再因氮饥饿或外部硝酸盐可用性降低而解除抑制。此外，该突变体在硝酸盐供应的根系中，也缺乏通常在另一部分根系氮剥夺时对硝酸盐吸收的补偿性上调。最后，在营养液中外源供应铵离子不能抑制突变体中的（15）硝酸盐流入，而在野生型中则会使其显著降低。这不能用突变体中铵离子吸收系统活性降低来解释。这些结果共同表明，AtNrt2.1和/或AtNrt2.2基因在高亲和力硝酸盐吸收的调控以及植物对环境中氮可用性的空间和时间变化的适应性反应中起关键作用。
