Disease relevance of narG

• A cosmid complementing narG mutants defective in nitrate reductase activity was isolated from a genomic library of Escherichia coli [1].

High impact information on narG

• Expression of narL does not require the fnr gene product, a pleiotropic activator that is required for full expression of narC, frd, and tor [2].
• DNase I footprinting studies revealed that IHF protects a 37-base pair region centered 125 base pairs 5' of the narG transcription site [3].
• Previous studies established that the first two genes in the operon narG and narH encode the alpha and beta subunits, respectively, while formation of the gamma subunit, cytochrome bNR, depends on expression of the promoter distal genes [4].
• Previous work has shown that nucleotide substitutions in two of these heptamers, centred at positions -195 and -89, severely reduce nitrate induction of narG operon expression in vivo and significantly interfere with NarL-DNA interactions in vitro [5].
• Substitutions in heptamers -185 and -101 affected narG operon induction only when the concentration of phospho-NarL was low (during growth in the presence of nitrite) [5].

Chemical compound and disease context of narG

• This places the tdk gene at approximately minute 27.35 on the E. coli W3110 chromosome, about 15 kb downstream from the narG locus and approximately 25 kb upstream of the trp operon [6].

Biological context of narG

• The position of the deletion end point relative to the translation start site for the first structural gene, narG, was defined by identifying the nucleotide sequence for the first 20 N-terminal amino acid residues of the alpha subunit of nitrate reductase [7].
• We conclude that the nar operon 5' regulatory region is divided into two distinct regions: the 100 to 150 bp immediately 5' to the narG gene include a transcriptional start site and the signals necessary for anaerobic expression of the operon, and an adjacent region of 50 to 400 bp is required for the stimulation of operon expression by nitrate [7].
• The narG mutants defective in nitrate reductase do not catalyze nitrosation, and the fnr gene is essential for nitrosation [8].
• A narG (nitrate reductase) mutation blocked the mutagenesis of the nfi mutant by nitrate but not by nitrite [9].
• The two membrane-bound respiratory nitrate reductases of Escherichia coli are encoded by distinct operons at two different loci, chlC and chlZ, on the chromosome [10].

Anatomical context of narG

• The nitrate reductase in the wild type was completely stable in vivo under inducing or noninducing conditions, whereas in the chlC and chlE mutants nitrate reductase was degraded extensively in both the cytoplasm and membranes, even under inducing conditions [11].

Associations of narG with chemical compounds

• In the present study we found that a molybdenum coeffector acted synergistically with nitrate in the regulation of frd and narC [12].
• In chlB mutants, which are known to accumulate the Mo cofactor because of its failure to be inserted as a prosthetic group into proteins such as nitrate reductase, nitrate repression of frd and induction of narC were also intensified by molybdate supplementation [12].

Physical interactions of narG

• The induction of the narC operon encoding the nitrate reductase is coupled to the repression of the frd operon encoding the fumarate reductase [12].

Other interactions of narG

• Protein fusions of lacZ with the N-terminal sequence of the narG gene were constructed so that beta-galactosidase formation was under the control of the nar promoter and one or both regulatory domains [13].
• From the nucleotide sequence of the narI region of the operon we conclude that, in addition to the narG and narH genes, the nar operon contains two other open reading frames (ORFs), ORF1 and ORF2, that encode proteins of 26.5 and 25.5 kilodaltons, respectively [14].
• The narGHJI operon, encoding nitrate reductaseA, is located in the chlC locus at 27 minutes, along with several functionally related genes: narK, encoding a nitrate/nitrite antiporter, and the narXL operon, encoding a nitrate-activated, two component regulatory system [15].
• The chlC locus is suggested to be the structural gene for nitrate reductase subunit A and chlE is suggested to be involved in the synthesis of the cytochrome b1 apoprotein [16].
• In light of these findings, prior models for the roles of nitrate and nitrite in control of narG and napF expression must be reconsidered [17].

References