Disease relevance of rpoS

• It has identified the CFA synthase gene as one of several rpoS-regulated genes of E. coli and has provided for the construction of strains in which proposed cellular functions of CFAs can be properly evaluated [1].
• Mutation of the phoP gene rendered Salmonella as sensitive to hydrogen peroxide as an rpoS mutant after growth in low Mg(2+) [2].
• We examined the transcription of Pseudomonas aeruginosa rpoS as to the growth of cells [3].
• The reason for this protective effect of polyP is the induction of HPII catalase and DNA repair enzymes as members of the rpoS regulon [4].
• We chose to start with examination of the rpoS gene since, among gram-negative bacteria, many genes needed for survival are regulated by RpoS, the stationary-phase sigma factor [5].

High impact information on rpoS

• This phenotype was conferred by mutations in rpoS, which encodes a putative stationary phase-specific sigma factor [6].
• In vitro, the expression of ospC and rpoS from flacp was dependent on the inducer isopropyl beta-D-thiogalactopyranoside and was unaffected by temperature or pH, conditions commonly used to mimic different aspects of the B. burgdorferi life cycle [7].
• Moreover, a moderate (threefold) further increase in the transcription rate of chromosomally encoded activated bgl operon alleles in an rpoS mutant can result in high (up to 50-fold increased) expression levels [8].
• DsrA also binds sequences in the 5'-untranslated leader region of rpoS mRNA, enhancing rpoS mRNA stability and RpoS translation [9].
• The sequence preceding the 5' end of rpoS mRNA showed poor homology to the consensus sequences of the previously known promoters [3].

Chemical compound and disease context of rpoS

• E. coli BJ4 and an isogenic BJ4 rpoS mutant were used to examine the influence of the rpoS gene on E. coli colonization of the streptomycin-treated mouse large intestine [10].
• These studies demonstrate the production of a glucose-phosphate by-product bactericidal to E. coli O157:H7 and the protective effects afforded by rpoS-regulated gene products [11].
• Negative control of rpoS expression by phosphoenolpyruvate: carbohydrate phosphotransferase system in Escherichia coli [12].
• When tetracycline was present, tetA(C) reduced acid tolerance, suppressed rpoS expression, and increased the concentration of total soluble proteins in stationary-phase Escherichia coli [13].
• Trehalose synthesis genes are controlled by the putative sigma factor encoded by rpoS and are involved in stationary-phase thermotolerance in Escherichia coli [14].

Biological context of rpoS

• A multicopy plasmid carrying rpoS strongly repressed expression of Esp proteins, suggesting that positive regulation by ClpXP is partially mediated through a negative effect of RpoS on LEE expression [15].
• Their expression is induced both by osmotic stress and by growth into the stationary phase and depend on the sigma factor encoded by rpoS (katF). rpoS is amber-mutated in E. coli K-12 and its DNA sequence varies among K-12 strains [16].
• Because of their well-established role in morphogenesis, we investigated the status of the penicillin-binding proteins (PBPs) in Escherichia coli wild-type and isogenic rpoS mutants [17].
• The failure of ppGpp-deficient strains to synthesize sigma s in response to these starvation regimens could indicate a general defect in gene expression rather than a specific dependence of rpoS expression on ppGpp [18].
• Our data suggest that PsrA is an important regulatory protein of Pseudomonas spp. involved in the regulatory cascade controlling rpoS gene regulation in response to cell density [19].

Anatomical context of rpoS

• rpoS gene function is a disadvantage for Escherichia coli BJ4 during competitive colonization of the mouse large intestine [10].
• The reduction in passage of the rpoS mutant was due to decreased AR, as administration of the mutant in 0.05 M phosphate buffer facilitated passage and increased the frequency of recovery in feces from 27 to 67% at a dose of 10(4) CFU [20].
• Effect of rpoS mutations on stress-resistance and invasion of brain microvascular endothelial cells in Escherichia coli K1 [21].
• We found that the cerebrospinal fluid isolates of E. coli K1 strains RS218 and IHE3034 have a nonsense mutation in their rpoS gene [21].
• The nlpD gene is located in an operon with rpoS on the Escherichia coli chromosome and encodes a novel lipoprotein with a potential function in cell wall formation [22].

Associations of rpoS with chemical compounds

• Wild-type bacteria were rapidly displaced by rpoS mutants in both glucose- and nitrogen-limited chemostat populations [23].
• The resultant rpoS mutant of P.putida, C1R1, showed reduced survival of carbon starvation and reduced cross-protection against other types of stress in cells starved for carbon, in particular after a challenge with ethanol [24].
• The induction of mdtEF by GlcNAc is not mediated by the evgSA, ydeO, gadX, and rpoS signaling pathways that have been known to regulate mdtEF expression [25].
• Polyamines, in particular putrescine, are involved in regulation of the rpoS expression by concentration-dependent stimulation at the levels of translation and stability of the protein sigmaS [26].

Regulatory relationships of rpoS

• We found that overexpression of relA activated the expression of rpoS in P. aeruginosa and led to premature, cell density-independent LasB elastase production [27].

Other interactions of rpoS

• Like in other gram-negative bacteria, a homolog of the nlpD gene was found upstream to the rpoS gene [24].

Analytical, diagnostic and therapeutic context of rpoS

• DksA appears to be involved in the expression of several genes in addition to rpoS based on two-dimensional SDS-PAGE analysis of whole-cell proteins [28].
• Electrophoretic mobility-shift assays yielded an apparent binding affinity of H-NS binding to curved DNA of approximately 1 microM, whereas binding to rpoS mRNA or DsrA RNA was approximately 3 microM [29].
• Patterns of resuscitation of S. enterica serovar Typhimurium rpoS mutants from water microcosms and heat stress were qualitatively similar, suggesting that the general stress response controlled by the sigma(s) subunit of RNA polymerase plays no role in autoinducer-dependent resuscitation [30].
• Sequence determination and comparison with rpoS from E. coli demonstrates a high degree of conservation, although significant differences are found within the extragenic regulatory regions [31].
• The intervening region between mutS and rpoS was amplified by long-range PCR, and the resulting amplicons varied substantially in length (7.8 to 14.2 kb) among pathogenic groups [32].

References