Southern Regional Collaborative Innovation Center for Grain and Oil Crops in China, College of Resources and Environmental Sciences, Hunan Agricultural University, Changsha, China 410128.
Center for Environmental Diagnostics and Bioremediation, University of West Florida, Pensacola, Florida 32514.
Plant Physiol. 2018 Dec;178(4):1473-1488. doi: 10.1104/pp.18.00410. Epub 2018 Oct 18.
A high concentration of ammonium (NH ) as the sole source of nitrogen in the growth medium often is toxic to plants. The nitrate transporter NRT1.1 is involved in mediating the effects of NH toxicity; however, the mechanism remains undefined. In this study, wild-type Arabidopsis ( Columbia-0 [Col-0]) and mutants ( and ) were grown hydroponically in NHNO and (NH)SO media to assess the function of NRT1.1 in NH stress responses. All the plants grew normally in medium containing mixed nitrogen sources, but Col-0 displayed more chlorosis and lower biomass and photosynthesis than the mutants in (NH)SO medium. Grafting experiments between Col-0 and further confirmed that NH toxicity is influenced by NRT1.1. In (NH)SO medium, NRT1.1 induced the expression of NH transporters, increasing NH uptake. Additionally, the activities of glutamine synthetase and glutamate synthetase in roots of Col-0 plants decreased and soluble sugar accumulated significantly, whereas pyruvate kinase-mediated glycolysis was not affected, all of which contributed to NH accumulation. By contrast, the mutants showed reduced NH accumulation and enhanced NH assimilation through glutamine synthetase, glutamate synthetase, and glutamate dehydrogenase. Moreover, the up-regulation of genes involved in ethylene synthesis and senescence in Col-0 plants treated with (NH)SO suggests that ethylene is involved in NH toxicity responses. This study showed that NH toxicity is related to a nitrate-independent signaling function of in Arabidopsis, characterized by enhanced NH accumulation and altered NH metabolism, which stimulates ethylene synthesis, leading to plant senescence.
高浓度的铵（NH ）作为生长培养基中氮的唯一来源通常对植物有毒。硝酸盐转运蛋白 NRT1.1 参与介导 NH 毒性的影响；然而，其机制尚不清楚。在这项研究中，野生型拟南芥（哥伦比亚-0 [Col-0]）和突变体（和）在含有 NHNO 和（NH ）SO 的水培介质中生长，以评估 NRT1.1 在 NH 胁迫反应中的功能。所有植物在含有混合氮源的培养基中正常生长，但与突变体相比，Col-0 在（NH ）SO 培养基中表现出更多的黄化和较低的生物量和光合作用。Col-0 和 之间的嫁接实验进一步证实，NH 毒性受 NRT1.1 影响。在（NH ）SO 培养基中，NRT1.1 诱导 NH 转运蛋白的表达，增加 NH 的吸收。此外，Col-0 植物根系中谷氨酰胺合成酶和谷氨酸合成酶的活性降低，可溶性糖显著积累，而丙酮酸激酶介导的糖酵解不受影响，所有这些都有助于 NH 的积累。相比之下，突变体通过谷氨酰胺合成酶、谷氨酸合成酶和谷氨酸脱氢酶显示出减少的 NH 积累和增强的 NH 同化。此外，Col-0 植物用（NH ）SO 处理后，参与乙烯合成和衰老的基因上调表明乙烯参与 NH 毒性反应。本研究表明，NH 毒性与拟南芥中 NRT1.1 的硝酸盐非依赖性信号功能有关，其特征是增强的 NH 积累和改变的 NH 代谢，这刺激乙烯的合成，导致植物衰老。
