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• W2017004777 abstract "Abstract Nitrate uptake by the roots is under systemic feedback repression by high nitrogen (N) status of the whole plant. The NRT2.1 gene, which encodes a NO3 − transporter involved in high-affinity root uptake, is a major target of this N signaling mechanism. Using transgenic Arabidopsis (Arabidopsis thaliana) plants expressing the pNRT2.1::LUC reporter gene (NL line), we performed a genetic screen to isolate mutants altered in the NRT2.1 response to high N provision. Three hni (for high nitrogen insensitive) mutants belonging to three genetic loci and related to single and recessive mutations were selected. Compared to NL plants, these mutants display reduced down-regulation of both NRT2.1 expression and high-affinity NO3 − influx under repressive conditions. Split-root experiments demonstrated that this is associated with an almost complete suppression of systemic repression of pNRT2.1 activity by high N status of the whole plant. Other mechanisms related to N and carbon nutrition regulating NRT2.1 or involved in the control of root SO4 − uptake by the plant sulfur status are not or are slightly affected. The hni mutations did not lead to significant changes in total N and NO3 − contents of the tissues, indicating that hni mutants are more likely regulatory mutants rather than assimilatory mutants. Nevertheless, hni mutations induce changes in amino acid, organic acid, and sugars pools, suggesting a possible role of these metabolites in the control of NO3 − uptake by the plant N status. Altogether, our data indicate that the three hni mutants define a new class of N signaling mutants specifically impaired in the systemic feedback repression of root NO3 − uptake." @default.
• W2017004777 created "2016-06-24" @default.
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• W2017004777 date "2010-05-06" @default.
• W2017004777 modified "2023-10-06" @default.
• W2017004777 title "Identification of Arabidopsis Mutants Impaired in the Systemic Regulation of Root Nitrate Uptake by the Nitrogen Status of the Plant " @default.
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• W2017004777 doi "https://doi.org/10.1104/pp.110.157354" @default.
• W2017004777 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2899898" @default.
• W2017004777 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20448103" @default.
• W2017004777 hasPublicationYear "2010" @default.
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