Regulation of<i>igaA</i>and the Rcs System by the MviA Response Regulator in<i>Salmonella enterica</i>

García-Calderón, Clara B.; Casadesús, Josep; Ramos‐Morales, Francisco

doi:10.1128/jb.01519-08

Cited by 8 publications

(9 citation statements)

References 89 publications

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“…The dynamics of the IS186 insertion in populations M3 and M4 suggest that this mutation was beneficial in the background with an IS1 insertion upstream of the homologue of igaA . Support for a selective advantage of this mutation is suggested by the observation that, in Salmonella, the transcription of igaA ( yrfF in E. coli ) is regulated by lon [37] .…”

Section: Resultsmentioning

confidence: 99%

The Genetic Basis of Escherichia coli Pathoadaptation to Macrophages

et al. 2013

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Antagonistic interactions are likely important driving forces of the evolutionary process underlying bacterial genome complexity and diversity. We hypothesized that the ability of evolved bacteria to escape specific components of host innate immunity, such as phagocytosis and killing by macrophages (MΦ), is a critical trait relevant in the acquisition of bacterial virulence. Here, we used a combination of experimental evolution, phenotypic characterization, genome sequencing and mathematical modeling to address how fast, and through how many adaptive steps, a commensal Escherichia coli (E. coli) acquire this virulence trait. We show that when maintained in vitro under the selective pressure of host MΦ commensal E. coli can evolve, in less than 500 generations, virulent clones that escape phagocytosis and MΦ killing in vitro, while increasing their pathogenicity in vivo, as assessed in mice. This pathoadaptive process is driven by a mechanism involving the insertion of a single transposable element into the promoter region of the E. coli yrfF gene. Moreover, transposition of the IS186 element into the promoter of Lon gene, encoding an ATP-dependent serine protease, is likely to accelerate this pathoadaptive process. Competition between clones carrying distinct beneficial mutations dominates the dynamics of the pathoadaptive process, as suggested from a mathematical model, which reproduces the observed experimental dynamics of E. coli evolution towards virulence. In conclusion, we reveal a molecular mechanism explaining how a specific component of host innate immunity can modulate microbial evolution towards pathogenicity.

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Section: Resultsmentioning

confidence: 99%

The Genetic Basis of Escherichia coli Pathoadaptation to Macrophages

et al. 2013

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“…Transposon mutagenesis was used to identify UmoB as a negative regulator of disA. The umoB gene product is a negative regulator of the Rcs phosphorelay and has been previously implicated by our lab and others in swarming regulation (15,18,19,20,21,22,23,24,25). Our data indicate that the effect of the umoB mutation on disA expression is dependent upon the Rcs phosphorelay system.…”

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confidence: 76%

Regulation of the Swarming Inhibitor disA in Proteus mirabilis

Szostek¹,

Rather²

2013

Journal of Bacteriology

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The disA gene encodes a putative amino acid decarboxylase that inhibits swarming in Proteus mirabilis. 5= rapid amplification of cDNA ends (RACE) and deletion analysis were used to identify the disA promoter. The use of a disA-lacZ fusion indicated that FlhD 4 C 2 , the class I flagellar master regulator, did not have a role in disA regulation. The putative product of DisA, phenethylamine, was able to inhibit disA expression, indicating that a negative regulatory feedback loop was present. Transposon mutagenesis was used to identify regulators of disA and revealed that umoB (igaA) was a negative regulator of disA. Our data demonstrate that the regulation of disA by UmoB is mediated through the Rcs phosphorelay. Proteus mirabilis is a Gram-negative bacillus and a causative agent of urinary tract infections in patients with abnormal urethras or requiring long-term catheterization (1, 2, 3). P. mirabilis is also known for its ability to swarm, a form of flagellummediated surface motility (4, 5). In liquid medium, P. mirabilis exists as a vegetative, peritrichously flagellated swimming cell. However, 3 to 4 h after being placed on a solid surface, the vegetative swimming cells differentiate into elongated, multinucleate, aseptate, hyperflagellated swarmer cells, as reviewed in reference 6. The swarmer cells aggregate to form multicellular rafts and move concentrically away from the central inoculum for approximately 1 to 2 h before dedifferentiating back to vegetative swimming cells (7). This cycle of differentiation and consolidation gives P. mirabilis its characteristic bull's-eye appearance on agar plates (4).Flagellar biogenesis is tightly controlled in P. mirabilis through a hierarchically tiered regulatory cascade consisting of class I, II, and III gene clusters (reviewed in reference 8). Class I consists solely of the flagellar master regulator flhDC. The FlhD 4 C 2 heterohexamer is the master swarming regulator and activates transcription of class II genes (9, 10, 11). Class II is comprised of genes needed to form the hook-basal body structure of the flagella as well as fliA, encoding the swarming sigma factor 28 , and flgM, the corresponding anti-sigma factor.28 is responsible for transcribing class III genes, including genes involved in chemotaxis, and the structural genes of the flagellar filament and motor. The energy expenditure to fully flagellate a swarmer cell and the cyclic aspect of swarming require that swarming be a tightly regulated process. Several signals inducing differentiation, such as the inhibition of flagellar rotation, accumulation of putrescine, and O-antigen contact with a solid surface, have been identified; however, the signals responsible for consolidation are poorly understood (12,13,14,15).A novel regulator of swarming, disA, that bears homology to aromatic amino acid decarboxylases was discovered by Stevenson et al. (16). Disruption of the disA gene resulted in a hyperswarming phenotype, whereas overexpression completely abolished swarming (16). Currently, the mechanism by whic...

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“…The phosphorylated RcsB protein can bind DNA and act as either a repressor or an activator (28). More recently, another input, UmoB (IgaA), has been implicated in controlling the Rcs system (4,5,12,13,17,30,31,42). The Rcs phosphorelay has been shown to respond to various stresses, such as those caused by perturbations in the cell envelope and peptidoglycan, or by osmotic stress (25,45).…”

mentioning

confidence: 99%

Role of the Umo Proteins and the Rcs Phosphorelay in the Swarming Motility of the Wild Type and an O-Antigen ( waaL ) Mutant of Proteus mirabilis

Morgenstein

Rather

2012

J Bacteriol

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Proteus mirabilis is a Gram-negative bacterium that exists as a short rod when grown in liquid medium, but during growth on surfaces it undergoes a distinct physical and biochemical change that culminates in the formation of a swarmer cell. How P. mirabilis senses a surface is not fully understood; however, the inhibition of flagellar rotation and accumulation of putrescine have been proposed to be sensory mechanisms.

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Regulation ofigaAand the Rcs System by the MviA Response Regulator inSalmonella enterica

Cited by 8 publications

References 89 publications

The Genetic Basis of Escherichia coli Pathoadaptation to Macrophages

The Genetic Basis of Escherichia coli Pathoadaptation to Macrophages

Regulation of the Swarming Inhibitor disA in Proteus mirabilis

Role of the Umo Proteins and the Rcs Phosphorelay in the Swarming Motility of the Wild Type and an O-Antigen ( waaL ) Mutant of Proteus mirabilis

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