NRT1.1-Related NH Toxicity Is Associated with a Disturbed Balance between NH Uptake and Assimilation.

Plant Physiol

Southern Regional Collaborative Innovation Center for Grain and Oil Crops in China, College of Resources and Environmental Sciences, Hunan Agricultural University, Changsha, China 410128

Published: December 2018

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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6288744PMC
http://dx.doi.org/10.1104/pp.18.00410DOI Listing

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