The FecI Extracytoplasmic-Function Sigma Factor of
            <i>Escherichia coli</i>
            Interacts with the β′ Subunit of RNA Polymerase

Mahren, Susanne; Braun, Volkmar

doi:10.1128/jb.185.6.1796-1802.2003

Cited by 44 publications

(35 citation statements)

References 51 publications

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“…In the absence of their cognate anti-factors, autoregulated factors can become constitutively active, resulting in increased abundance of the factor. However, in some cases, ECF factors exhibit reduced activity and abundance in the absence of their cognate anti-factors, which are thought to stabilize and protect the factor from degradation (39,40). Alternatively, anti-factors can also promote the proteolysis of their cognate factors (41).…”

Section: Resultsmentioning

confidence: 99%

σ Factor and Anti-σ Factor That Control Swarming Motility and Biofilm Formation in Pseudomonas aeruginosa

2016

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Pseudomonas aeruginosa is capable of causing a variety of acute and chronic infections. Here, we provide evidence that sbrR (PA2895), a gene previously identified as required during chronic P. aeruginosa respiratory infection, encodes an anti-factor that inhibits the activity of its cognate extracytoplasmic-function factor, SbrI (PA2896). Bacterial two-hybrid analysis identified an N-terminal region of SbrR that interacts directly with SbrI and that was sufficient for inhibition of SbrI-dependent gene expression. We show that SbrI associates with RNA polymerase in vivo and identify the SbrIR regulon. In cells lacking SbrR, the SbrI-dependent expression of muiA was found to inhibit swarming motility and promote biofilm formation. Our findings reveal SbrR and SbrI as a novel set of regulators of swarming motility and biofilm formation in P. aeruginosa that mediate their effects through muiA, a gene not previously known to influence surface-associated behaviors in this organism. IMPORTANCEThis study characterizes a factor/anti-factor system that reciprocally regulates the surface-associated behaviors of swarming motility and biofilm formation in the opportunistic pathogen Pseudomonas aeruginosa. We present evidence that SbrR is an anti-factor specific for its cognate factor, SbrI, and identify the SbrIR regulon in P. aeruginosa. We find that cells lacking SbrR are severely defective in swarming motility and exhibit enhanced biofilm formation. Moreover, we identify muiA (PA1494) as the SbrI-dependent gene responsible for mediating these effects. SbrIR have been implicated in virulence and in responding to antimicrobial and cell envelope stress. SbrIR may therefore represent a stress response system that influences the surface behaviors of P. aeruginosa during infection.T he Gram-negative bacterium Pseudomonas aeruginosa is an opportunistic human pathogen notorious for being the principal cause of morbidity and mortality in cystic fibrosis (CF) patients (1). In patients with CF, chronic pulmonary colonization by P. aeruginosa leads to chronic inflammation, progressive loss of lung function, and eventually respiratory failure and death (1). P. aeruginosa is also the fifth leading cause of nosocomial infections overall in the United States and is the second most common cause of ventilator-associated pneumonia (VAP) and catheter-associated urinary tract infections (CAUTI) (2, 3). In patients with VAP or CAUTI, P. aeruginosa grows as a biofilm on endotracheal tubes and catheters, respectively (4-6). In addition, P. aeruginosa is thought to persist as a biofilm in the CF lung (7). P. aeruginosa biofilms are associated with chronic infection and exhibit increased antibiotic resistance and resistance to clearance by the immune system (8). Thus, the ability to form biofilms contributes significantly to the clinical burden of P. aeruginosa infection.In P. aeruginosa, growth as a biofilm is inversely regulated with a cooperative form of multicellular surface motility called swarming (9-12). Swarming motility is flagell...

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Section: Resultsmentioning

confidence: 99%

σ Factor and Anti-σ Factor That Control Swarming Motility and Biofilm Formation in Pseudomonas aeruginosa

2016

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“…This in turn correlates with the fact that many members of the TetR family are found among microbes with abundant extracytoplasmic function sigma factors (52,227,236,277,444).…”

Section: Identification Of Tetr Family Members In Dna and Protein Datmentioning

confidence: 99%

The TetR Family of Transcriptional Repressors

Ramos

Martínez-Bueno

Molina‐Henares

et al. 2005

Microbiol Mol Biol Rev

988

1,133

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We have developed a general profile for the proteins of the TetR family of repressors. The stretch that best defines the profile of this family is made up of 47 amino acid residues that correspond to the helix-turn-helix DNA binding motif and adjacent regions in the three-dimensional structures of TetR, QacR, CprB, and EthR, four family members for which the function and three-dimensional structure are known. We have detected a set of 2,353 nonredundant proteins belonging to this family by screening genome and protein databases with the TetR profile. Proteins of the TetR family have been found in 115 genera of gram-positive, α-, β-, and γ-proteobacteria, cyanobacteria, and archaea. The set of genes they regulate is known for 85 out of the 2,353 members of the family. These proteins are involved in the transcriptional control of multidrug efflux pumps, pathways for the biosynthesis of antibiotics, response to osmotic stress and toxic chemicals, control of catabolic pathways, differentiation processes, and pathogenicity. The regulatory network in which the family member is involved can be simple, as in TetR (i.e., TetR bound to the target operator represses tetA transcription and is released in the presence of tetracycline), or more complex, involving a series of regulatory cascades in which either the expression of the TetR family member is modulated by another regulator or the TetR family member triggers a cell response to react to environmental insults. Based on what has been learned from the cocrystals of TetR and QacR with their target operators and from their three-dimensional structures in the absence and in the presence of ligands, and based on multialignment analyses of the conserved stretch of 47 amino acids in the 2,353 TetR family members, two groups of residues have been identified. One group includes highly conserved positions involved in the proper orientation of the helix-turn-helix motif and hence seems to play a structural role. The other set of less conserved residues are involved in establishing contacts with the phosphate backbone and target bases in the operator. Information related to the TetR family of regulators has been updated in a database that can be accessed at www.bactregulators.org

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“…FecA not only mediates the uptake of ferric citrate but also transmits a signal through the cytoplasmic membrane protein FecR, which subsequently activates the FecI factor (69,157,158,247,324). FecI then associates with RNAP and activates transcription of the fecABCDE operon (23,395). FecB serves as the PBP that shuttles ferric citrate to the cytoplasmic ABC transporter, which is composed of FecCDE (69,566).…”

Section: Iron Uptake and Transportmentioning

confidence: 99%

Change Is Good: Variations in Common Biological Mechanisms in the Epsilonproteobacterial GeneraCampylobacterandHelicobacter

Gilbreath

Cody

Merrell

et al. 2011

Microbiol Mol Biol Rev

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SUMMARY Microbial evolution and subsequent species diversification enable bacterial organisms to perform common biological processes by a variety of means. The epsilonproteobacteria are a diverse class of prokaryotes that thrive in diverse habitats. Many of these environmental niches are labeled as extreme, whereas other niches include various sites within human, animal, and insect hosts. Some epsilonproteobacteria, such as Campylobacter jejuni and Helicobacter pylori , are common pathogens of humans that inhabit specific regions of the gastrointestinal tract. As such, the biological processes of pathogenic Campylobacter and Helicobacter spp. are often modeled after those of common enteric pathogens such as Salmonella spp. and Escherichia coli . While many exquisite biological mechanisms involving biochemical processes, genetic regulatory pathways, and pathogenesis of disease have been elucidated from studies of Salmonella spp. and E. coli , these paradigms often do not apply to the same processes in the epsilonproteobacteria. Instead, these bacteria often display extensive variation in common biological mechanisms relative to those of other prototypical bacteria. In this review, five biological processes of commonly studied model bacterial species are compared to those of the epsilonproteobacteria C. jejuni and H. pylori . Distinct differences in the processes of flagellar biosynthesis, DNA uptake and recombination, iron homeostasis, interaction with epithelial cells, and protein glycosylation are highlighted. Collectively, these studies support a broader view of the vast repertoire of biological mechanisms employed by bacteria and suggest that future studies of the epsilonproteobacteria will continue to provide novel and interesting information regarding prokaryotic cellular biology.

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The FecI Extracytoplasmic-Function Sigma Factor of Escherichia coli Interacts with the β′ Subunit of RNA Polymerase

Cited by 44 publications

References 51 publications

σ Factor and Anti-σ Factor That Control Swarming Motility and Biofilm Formation in Pseudomonas aeruginosa

σ Factor and Anti-σ Factor That Control Swarming Motility and Biofilm Formation in Pseudomonas aeruginosa

The TetR Family of Transcriptional Repressors

Change Is Good: Variations in Common Biological Mechanisms in the Epsilonproteobacterial GeneraCampylobacterandHelicobacter

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