Disease relevance of rpoN

• Novel proteins of the phosphotransferase system encoded within the rpoN operon of Escherichia coli. Enzyme IIANtr affects growth on organic nitrogen and the conditional lethality of an erats mutant [1].
• Significant homology was evident comparing the rpoN sequence of S. violacea with that of Escherichia coli (62.8% identity), Vibrio anguillarum (61.7% identity) and Pseudomonas putida (57.0% identity) [2].
• The cloned Azotobacter genes also complemented Klebsiella pneumoniae mutants and hybridized to K. pneumoniae ntrA, ntrC and glnA gene probes [3].
• The ntrA, ntrB and ntrC products are responsible for regulating the transcription of many genes involved in the assimilation of poor nitrogen sources in enteric bacteria [3].
• In the present study we cloned the Pseudomonas putida rpoN gene and identified its gene product as a protein with an apparent molecular weight of 78,000 [4].

High impact information on rpoN

• In response to ammonia starvation, the product of the glnG gene activates transcription of the nifLA operon; this activation is dependent on the product of glnF (ref. 4). The nifA gene product is in turn required for transcription of all the other nif genes, including the nifHDK operon which codes for the subunits of nitrogenase [5].
• However, ntrC is not required for nitrogen fixation by A. vinelandii, in contrast with K. pneumoniae where both ntrA and ntrC are essential [3].
• These mutants show that both ntrA and ntrC are required for the utilization of nitrate as a nitrogen source [3].
• Genes analogous to ntrA and ntrC were isolated from an A. vinelandii gene library by complementation of Escherichia coli mutants [3].
• One truncates rpoN while the second disrupts another gene (ptsN) in the rpoN operon and does not affect classical nitrogen regulation [1].

Chemical compound and disease context of rpoN

• The ntrA gene of Thiobacillus ferrooxidans was cloned by complementation of an Escherichia coli ntrA mutant that was unable to produce gas via the sigma 54 (NtrA)-dependent formate hydrogenlyase pathway [6].

Biological context of rpoN

• Plasmid clones of ptsN prevent suppression by either disruption mutation indicating that this gene is important for lethality caused by erats. rpoN and six neighboring genes were sequenced and compared with sequences in the database [1].
• Although a sigma54 consensus sequence was identified in the region between S1 and S2, a corresponding transcript was not detected, and a rpoN mutant of R. meliloti was able to utilize 3-hydroxybutyrate as a sole carbon source [7].
• The nucleotide sequence of the region extending 2.1 kb downstream of rpoN was also determined [8].
• These results identify the glnF product as a new sigma factor specifically required for the transcription of nitrogen-regulated and of nitrogen-fixation promoters [9].
• Inactivation of transcription factor sigma54, encoded by rpoN (glnF), restores high-temperature growth in Luria-Bertani (LB) medium to strains containing the heat-sensitive cell division mutation ftsZ84 [10].

Anatomical context of rpoN

• To test this hypothesis, we studied the adherence to human endothelial cells in primary culture of the piliated P. aeruginosa strain PAK and of two isogenic nonpiliated strains: PAK/p-, which carries a mutation in the pilin structural gene, and PAK-N1, a mutant defective in the regulatory rpoN gene [11].

Associations of rpoN with chemical compounds

• The bacterial rpoN operon codes for sigma 54, which is the key sigma factor that, under nitrogen starvation conditions, activates the transcription of genes needed to assimilate ammonia and glutamate [12].
• Streptomycin resistance was also obtained in an rpoN mutant of P. putida KT2440 containing constructs with the intact bkd promoter, indicating that the bkd operon does not require the rpoN sigma factor for expression [13].
• Investigations of rpoN-negative mutants of related strains revealed that polyhydroxyalkanoate accumulation from gluconate required an intact rpoN locus in P. aeruginosa [14].

Other interactions of rpoN

• Escherichia coli rpoN mutants lack sigma 54 and are therefore unable to initiate the transcription of glnA at glnAp2, which is required for the production of a high intracellular concentration of glutamine synthetase [15].
• All the lineages examined, however, contain the intact forms of sigma70 (sigmaD, the rpoD gene product) and sigma54 (sigmaN, the rpoN gene product) [16].
• The role of ntrA and ntrC in A. vinelandii was established by using Tn5 insertions in the cloned genes to construct mutants by marker exchange [3].
• Both the glnF null mutation and an elevated copy number of the relA gene similarly affect transcription from the upstream (pQ) promoters of the ftsQAZ operon, and both of these genetic conditions increase the steady-state level of the FtsZ84 protein [10].
• These mutations were located by transduction near min 69 on the E. coli K-12 genetic map, between argG and glnF [17].

Analytical, diagnostic and therapeutic context of rpoN

• Cloning and sequence analysis of the ntrA (rpoN) gene of Pseudomonas putida [18].

References