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H356A
the mutation results in complete loss of nitrate binding ability
T101A
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inactivation of the high-affinity component of the transporter by preventing phosphorylation at Thr101
T101D
the variant shows increased nitrate uptake of approximately 2.8fold compared to the wild type enzyme
F145A
the mutant displays binding to both nitrate and nitrite
F265A
the mutant retains very weak binding to nitrate but not to nitrite
F367A
the mutation abrogates binding to both nitrate and nitrite
F47A
the mutation abrogates binding to both nitrate and nitrite
N173A
the mutant retains some binding to substrate, albeit drastically reduced in comparison to the wild type
R303A
the mutation completely abrogates binding to nitrate or nitrite
R87A
the mutation completely abrogates binding to nitrate or nitrite
W50A
the mutation abrogates binding to both nitrate and nitrite
Y261A,
the mutation completely abrogates binding to nitrate or nitrite
A145G
the mutant shows wild type activity
A92G
the mutant shows wild type activity
C309S
the mutant shows wild type activity
C378S
the mutant shows wild type activity
D267G
the mutant shows reduced activity compared to the wild type enzyme
F114S
the mutant shows reduced activity compared to the wild type enzyme
F19S
the mutant shows reduced activity compared to the wild type enzyme
G140S
the mutant shows reduced activity compared to the wild type enzyme
G315S
the mutant shows reduced activity compared to the wild type enzyme
G69S
the mutant shows reduced activity compared to the wild type enzyme
G70P
the mutant shows wild type activity
G89S
the mutant shows wild type activity
I118L
the mutant shows wild type activity
L8V
the mutant shows wild type activity
P50S
the mutant shows reduced activity compared to the wild type enzyme
P84T
the mutant shows reduced activity compared to the wild type enzyme
R129S
the mutant shows wild type activity
T78S
the mutant shows wild type activity
Y97S
the mutant shows wild type activity
C309S
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the mutant shows wild type activity
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G140S
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the mutant shows reduced activity compared to the wild type enzyme
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G69S
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the mutant shows reduced activity compared to the wild type enzyme
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T78S
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the mutant shows wild type activity
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DELTA232-286
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enzyme does not disappear in response to glutamine
K243R
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no effect on down-regulation by glutamine
K243R/K253R
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reduced down-regulation in response to glutamine
K243R/K253R/K270R
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no ubiquitinylation, strongly reduced down-regulation in response to glutamine
K253R
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reduced down-regulation in response to glutamine
K253R/K270R
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reduced down-regulation in response to glutamine
K270R
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reduced down-regulation in response to glutamine
additional information
construction of a knockout mutant, no effect on plant growth, no changes in nitrate uptake upon acid load or medium acidification
additional information
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mutation of the NRT1.5 nitrate transporter causes defective root-to-shoot nitrate transport, knockdown or knockout mutations of NRT1.5 reduces the amount of nitrate transported from the root to the shoot, Root and shoot nitrate contents of antisense NRT1.5 plants, overview. T-DNA-tagged mutants nrt1.5-1 and nrt1.5-2 are defective in long-distance transport of nitrate but not of sulfate or phosphate
additional information
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a line expressing the auxin-inducible DR5::GUS reporter gene is crossed with the chl1-5 knockout mutant for NRT1.1. Mutation of NRT1.1 does not affect expression of DR5::GUS in plants supplied with 1 mM NO3, but dramatically increases it in plants either grown in the absence of NO3- or supplied with a low external NO3- concentration. Absence of a functional NRT1.1 transporter prevents the decrease of DR5::GUS expression in response to removal or lowered supply of NO3-, leading to a high DR5 activity regardless of the presence of an N source, phenotype, overview
additional information
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isolation of three high nitrogen insensitive mutants, belonging to three genetic loci and related to single and recessive mutations, that display reduced downregulation of both NRT2.1 expression and high-affinity NO3- influx under repressive conditions. associated with an almost complete suppression of systemic repression of pNRT2.1 activity by high N status of the whole plant. The three hni mutants define a class of N signaling mutants specifically impaired in the systemic feedback repression of root NO3- uptake, molecular effects of the mutations and phenotypes, detailed overview. pNRT2.1::LUC is a good marker for NRT2.1 expression
additional information
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generation of several mutants devoid of NAR2.1, e.g. Atnar2.1-35S:NAR2.1-myc mutant, complementation by expression of wild-type NAR2.1, phenotypes, overview
additional information
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mutation of the NRT1.5 nitrate transporter causes defective root-to-shoot nitrate transport, knockdown or knockout mutations of NRT1.5 reduces the amount of nitrate transported from the root to the shoot, Root and shoot nitrate contents of antisense NRT1.5 plants, overview. T-DNA-tagged mutants nrt1.5-1 and nrt1.5-2 are defective in long-distance transport of nitrate but not of sulfate or phosphate
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additional information
nitrate uptake is restored in mutant chl1-5 plants by expression of the wild-type enzyme using the 35S::BcNRT1 construct
additional information
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construction of deletion mutants, NarK1 mutant grows almost normally, while NarK2 mutant shows strongly reduced generation times under nitrate-dependent anaerobic growth conditions, almost no growth of the NarK1/NarK2 double mutant, impaired growth can be restored by expression of the narK gene from Escherichia coli K-12
additional information
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the NA3 mutant of strain PCC7942, constructed by deleting the nrtABCD genes from the nirA operon, is defective in the active transport of nitrate, an insertional mutant of NA3 is constructed for each of the four genes and analyzed for its nitrite transport ability, overview
additional information
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the NA3 mutant of strain PCC7942, constructed by deleting the nrtABCD genes from the nirA operon, is defective in the active transport of nitrate, an insertional mutant of NA3 is constructed for each of the four genes and analyzed for its nitrite transport ability, overview
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