Transcript Profiling in thechl1-5Mutant of Arabidopsis Reveals a Role of the Nitrate Transporter NRT1.1 in the Regulation of Another Nitrate Transporter, NRT2.1[W]
Open Access
- 1 September 2004
- journal article
- Published by Oxford University Press (OUP) in THE PLANT CELL ONLINE
- Vol. 16 (9), 2433-2447
- https://doi.org/10.1105/tpc.104.024380
Abstract
Arabidopsis thaliana mutants deficient for the NRT1.1 NO3− transporter display complex phenotypes, including lowered NO3− uptake, altered development of nascent organs, and reduced stomatal opening. To obtain further insight at the molecular level on the multiple physiological functions of NRT1.1, we performed large-scale transcript profiling by serial analysis of gene expression in the roots of the chl1-5 deletion mutant of NRT1.1 and of the Columbia wild type. Several hundred genes were differentially expressed between the two genotypes, when plants were grown on NH4NO3 as N source. Among these genes, the N satiety-repressed NRT2.1 gene, encoding a major component of the root high-affinity NO3− transport system (HATS), was found to be strongly derepressed in the chl1-5 mutant (as well as in other NRT1.1 mutants). This was associated with a marked stimulation of the NO3− HATS activity in the mutant, suggesting adaptive response to a possible N limitation resulting from NRT1.1 mutation. However, derepression of NRT2.1 in NH4NO3-fed chl1-5 plants could not be attributed to lowered production of N metabolites. Rather, the results show that normal regulation of NRT2.1 expression is strongly altered in the chl1-5 mutant, where this gene is no more repressible by high N provision to the plant. This indicates that NRT1.1 plays an unexpected but important role in the regulation of both NRT2.1 expression and NO3− HATS activity. Overexpression of NRT2.1 was also found in wild-type plants supplied with 1 mM NH4+ plus 0.1 mM NO3−, a situation where NRT1.1 is likely to mediate very low NO3− transport. Thus, we suggest that it is the lack of NRT1.1 activity, rather than the absence of this transporter, that derepresses NRT2.1 expression in the presence of NH4+. Two hypotheses are discussed to explain these results: (1) NRT2.1 is upregulated by a NO3− demand signaling, indirectly triggered by lack of NRT1.1-mediated uptake, which overrides feedback repression by N metabolites, and (2) NRT1.1 plays a more direct signaling role, and its transport activity generates an unknown signal required for NRT2.1 repression by N metabolites. Both mechanisms would warrant that either NRT1.1 or NRT2.1 ensure significant NO3− uptake in the presence of NH4+ in the external medium, which is crucial to prevent the detrimental effects of pure NH4+ nutrition.Keywords
This publication has 57 references indexed in Scilit:
- Regulation of Root Ion Transporters by Photosynthesis: Functional Importance and Relation with HexokinaseTHE PLANT CELL ONLINE, 2003
- The Nitrate Transporter AtNRT1.1 (CHL1) Functions in Stomatal Opening and Contributes to Drought Susceptibility in ArabidopsisTHE PLANT CELL ONLINE, 2002
- Nitrate regulation of metabolism and growthCurrent Opinion in Plant Biology, 1999
- Three Functional Transporters for Constitutive, Diurnally Regulated, and Starvation-Induced Uptake of Ammonium into Arabidopsis RootsTHE PLANT CELL ONLINE, 1999
- Molecular and physiological aspects of nitrate uptake in plantsTrends in Plant Science, 1998
- Expression studies of Nrt2:1Np, a putative high‐affinity nitrate transporter: evidence for its role in nitrate uptakeThe Plant Journal, 1998
- The herbicide sensitivity gene CHL1 of arabidopsis encodes a nitrate-inducible nitrate transporterCell, 1993
- Studies of the Regulation of Nitrate Influx by Barley Seedlings Using 13NO3−Plant Physiology, 1989
- Uptake of chlorate and other ions in seedlings of the nitrate‐uptake mutant B1 of Arabidopsis thalianaPhysiologia Plantarum, 1986
- Isolation and characterization of chlorate-resistant mutants of Arabidopsis thalianaMutation research. Reviews in mutation research, 1973