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PubMed2002

Quorum sensing is not required for twitching motility in Pseudomonas aeruginosa.

It has been reported that mutations in the quorum-sensing genes lasI and rhlI in Pseudomonas aeruginosa result in, among many other things, loss of twitching motility (A. Glessner, R. S. Smith, B. H. Iglewski, and J. B. Robinson, J. Bacteriol. 181:1623-1629, 1999). We constructed knockouts of lasI and rhlI and the corresponding regulatory genes lasR and rhlR and found no effect on twitching motility. However, twitching-defective variants accumulated during culturing of lasI and rhlI mutants. Further analysis showed that the stable twitching-defective variants of lasI and rhlI mutants had arisen as a consequence of secondary mutations in vfr and algR, respectively, both of which encode key regulators affecting a variety of phenotypes, including twitching motility. In addition, when grown in shaking broth culture, lasI and rhlI mutants, but not the wild-type parent, also accumulated unstable variants that lacked both twitching motility and swimming motility and appeared to be identical in phenotype to the S1 and S2 variants that were recently reported to occur at high frequencies in P. aeruginosa strains grown as a biofilm or in static broth culture (E. Deziel, Y. Comeau, and R. Villemur, J. Bacteriol. 183:1195-1204, 2001). These results indicate that mutations in one regulatory system may create distortions that select during subsequent culturing for compensatory mutations in other regulatory genes within the cellular network. This problem may have compromised some past studies of regulatory hierarchies controlled by quorum sensing and of bacterial regulatory systems in general.

Bacterial Proteins↗

PubMed2002

Control of the AcrAB multidrug efflux pump by quorum-sensing regulator SdiA.

SdiA is an Escherichia coli protein that regulates cell division in a cell density-dependent, or quorum-sensing, manner. We report that SdiA also controls multidrug resistance by positively regulating the multidrug resistance pump AcrAB. Overproduction of SdiA confers multidrug resistance and increased levels of AcrAB. Conversely, sdiA null mutants are hypersensitive to drugs and have decreased levels of AcrB protein. Our findings provide a link between quorum sensing and multidrug efflux. Combined with previously published reports, our data support a model in which a role of drug efflux pumps is to mediate cell-cell communication in response to cell density. Xenobiotics expelled by pumps may resemble the communication molecules that they normally efflux.

Bacterial Proteins↗

PubMed2001

Inhibition of quorum sensing by a Pseudomonas aeruginosa dksA homologue.

The Pseudomonas aeruginosa las (lasR-lasI) and rhl (rhlR-rhlI) quorum-sensing systems regulate the expression of several virulence factors, including elastase and rhamnolipid. P. aeruginosa strain PR1-E4 is a lasR deletion mutant that contains a second, undefined mutation which allows production of elastase and rhamnolipid despite a nonfunctional las system. We have previously shown that this strain accomplishes this by increasing the expression of the autoinducer synthase gene rhlI. In this report, we show that the elastolytic phenotype of mutant PR1-E4 can be complemented with a P. aeruginosa homologue of the Escherichia coli dnaK mutation suppressor gene dksA. When supplied in trans on a multicopy plasmid, this gene completely suppressed elastase production by mutant PR1-E4. Cloning and Northern blot analysis revealed that dksA was neither mutated nor less transcribed in mutant PR1-E4. When overexpressed, dksA also reduced rhamnolipid production by both mutant PR1-E4 and the wild type, PAO1. Using Northern blot analysis and lacZ reporter fusions, we show that dksA inhibits rhlI, rhlAB, and lasB transcription. Exogenous N-butyryl-L-homoserine lactone overcame the reduced expression of rhlI and restored rhlAB and lasB expression, as well as elastase production. Our results suggest that the overproduction of the P. aeruginosa DksA homologue inhibits quorum-sensing-dependent virulence factor production by downregulating the transcription of the autoinducer synthase gene rhlI.

Bacterial Proteins↗

PubMed2003

The Vibrio fischeri quorum-sensing systems ain and lux sequentially induce luminescence gene expression and are important for persistence in the squid host.

Bacterial quorum sensing using acyl-homoserine lactones (acyl-HSLs) as cell-density dependent signalling molecules is important for the transcriptional regulation of many genes essential in the establishment and the maintenance of bacteria-host associations. Vibrio fischeri, the symbiotic partner of the Hawaiian bobtail squid Euprymna scolopes, possesses two distinct acyl-HSL synthase proteins, LuxI and AinS. Whereas the cell density-dependent regulation of luminescence by the LuxI-produced signal is a well-described phenomenon, and its role in light organ symbiosis has been defined, little is known about the ain system. We have investigated the impact of the V. fischeri acyl-HSL synthase AinS on both luminescence and symbiotic colonization. Through phenotypic studies of V. fischeri mutants we have found that the AinS-signal is the predominant inducer of luminescence expression in culture, whereas the impact of the LuxI-signal is apparent only at the high cell densities occurring in symbiosis. Furthermore, our studies revealed that ainS regulates activities essential for successful colonization of E. scolopes, i.e. the V. fischeri ainS mutant failed to persist in the squid light organ. Mutational inactivation of the transcriptional regulator protein LuxO in the ainS mutant partially or completely reversed all the observed phenotypes, demonstrating that the AinS-signal regulates expression of downstream genes through the inactivation of LuxO. Taken together, our results suggest that the two quorum-sensing systems in V. fischeri, ain and lux, sequentially induce the expression of luminescence genes and possibly other colonization factors.

Animals↗

PubMed2000

The regulatory locus cinRI in Rhizobium leguminosarum controls a network of quorum-sensing loci.

N-(3-hydroxy-7-cis-tetradecenoyl)-L-homoserine lactone (3OH, C14:1-HSL) is a quorum-sensing signalling molecule produced by Rhizobium leguminosarum. It is unusual in that it inhibits the growth of several strains of R. leguminosarum and was previously known as 'small bacteriocin'. The cinRI locus responsible for the production of 3OH,C14:1-HSL has been characterized; it is predicted to be on the chromosome, based on DNA hybridization. The cinR and cinI genes are in different transcriptional units, separated by a predicted transcription terminator. CinR regulates cinI expression to a very high level in a cell-density dependent manner, and cinI expression is positively autoregulated by 3OH,C14:1-HSL, the only identified N-acyl homoserine lactone (AHL) produced by CinI. No other AHLs were identified that strongly induced cinI expression. Mutation of cinI or cinR abolishes the production of 3OH,C14:1-HSL and also reduces the production of several other AHLs. This is thought to result from the expression of three other AHL production loci being affected by the absence of 3OH,C14:1-HSL. AHLs produced by these other loci include N-hexanoyl- and N-octanoyl-L-homoserine lactones and, unexpectedly, N-heptanoyl-L-homoserine lactone (C7-HSL). The expression of the rhiI gene on the symbiotic plasmid is greatly reduced in a cinI mutant, and the major regulatory effect appears to be mediated at least in part as a result of an effect on expression of RhiR, the regulator of rhiI. Thus, cinR and cinI appear to be at the top of a regulatory cascade or network that influences several AHL-regulated quorum-sensing loci. The expression of cinI-lacZ fusions is significantly reduced (but not abolished) when the symbiosis plasmid pRL1JI is present, resulting in a reduction in the level of 3OH,C14:1-HSL produced. Mutation of cinI had little effect on growth or nodulation. However, plasmid transfer was affected, and the results obtained indicate that 3OH,C14:1-HSL produced by either the donor or the recipient in mating experiments can stimulate transfer of pRL1JI.

4-Butyrolactone↗

PubMed2025

Quorum sensing in Saccharomyces cerevisiae brewing strains: effects of 2-phenylethanol on proteomic, lipidomic, and metabolomic profile.

Quorum sensing (QS) is a known mechanism by which microbial populations adjust gene expression and coordinate community-wide social behaviors based on the proximate population density. This regulatory system has garnered significant interest in both scientific research and the food industry. However, a central question remains whether industrial strains of Saccharomyces cerevisiae, the yeast species predominantly utilized in brewing, employ quorum signalling mechanisms similar to those observed in laboratory strains and other fungi. Despite the potential relevance of microbial social behavior regulators to brewing practices, studies examining QS in Saccharomyces spp. are limited. In this investigation, three industrial brewing strains of S. cerevisiae were cultivated on SLAD (nitrogen-restrictive) and SHAD (nitrogen-sufficient) agar media supplemented with 200 μM of the aromatic alcohol 2-phenylethanol (2-PE) over 72 h at 24°C. Subsequent analyses of the harvested biomass included proteomic, lipidomic, and metabolomic assessments. Results indicated that two of the industrial strains showed minimal differences in their profiles upon exposure to 2-PE, while the third strain exhibited significant differences. These findings imply that the impact of the QS molecule 2-PE on the proteome, lipidome, and metabolome of industrial S. cerevisiae may be strain-specific rather than universally applicable to the species.

Quorum Sensing↗

PubMed2007

Rhomboid protease AarA mediates quorum-sensing in Providencia stuartii by activating TatA of the twin-arginine translocase.

The Providencia stuartii AarA protein is a member of the rhomboid family of intramembrane serine proteases and is required for the production of an unknown quorum-sensing molecule. In a screen to identify rhomboid-encoding genes from Proteus mirabilis, tatA was identified as a multicopy suppressor and restored extracellular signal production as well as complementing all other phenotypes of a Prov. stuartii aarA mutant. TatA is a component of the twin-arginine translocase (Tat) protein secretion pathway and likely forms a secretion pore. By contrast, the native tatA gene of Prov. stuartii in multicopy did not suppress an aarA mutation. We find that TatA in Prov. stuartii has a short N-terminal extension that was atypical of TatA proteins from most other bacteria. This extension was proteolytically removed by AarA both in vivo and in vitro. A Prov. stuartii TatA protein missing the first 7 aa restored the ability to rescue the aarA-dependent phenotypes. To verify that loss of the Tat system was responsible for the various phenotypes exhibited by an aarA mutant, a tatC-null allele was constructed. The tatC mutant exhibited the same phenotypes as an aarA mutant and was epistatic to aarA. These data provide a molecular explanation for the requirement of AarA in quorum-sensing and uncover a function for the Tat protein export system in the production of secreted signaling molecules. Finally, TatA represents a validated natural substrate for a prokaryotic rhomboid protease.

Amino Acid Sequence↗

PubMed2002

A quorum-sensing signaling system essential for genetic competence in Streptococcus mutans is involved in biofilm formation.

In a previous study, a quorum-sensing signaling system essential for genetic competence in Streptococcus mutans was identified, characterized, and found to function optimally in biofilms (Li et al., J. Bacteriol. 183:897-908, 2001). Here, we demonstrate that this system also plays a role in the ability of S. mutans to initiate biofilm formation. To test this hypothesis, S. mutans wild-type strain NG8 and its knockout mutants defective in comC, comD, comE, and comX, as well as a comCDE deletion mutant, were assayed for their ability to initiate biofilm formation. The spatial distribution and architecture of the biofilms were examined by scanning electron microscopy and confocal scanning laser microscopy. The results showed that inactivation of any of the individual genes under study resulted in the formation of an abnormal biofilm. The comC mutant, unable to produce or secrete a competence-stimulating peptide (CSP), formed biofilms with altered architecture, whereas the comD and comE mutants, which were defective in sensing and responding to the CSP, formed biofilms with reduced biomass. Exogenous addition of the CSP and complementation with a plasmid containing the wild-type comC gene into the cultures restored the wild-type biofilm architecture of comC mutants but showed no effect on the comD, comE, or comX mutant biofilms. The fact that biofilms formed by comC mutants differed from the comD, comE, and comX mutant biofilms suggested that multiple signal transduction pathways were affected by CSP. Addition of synthetic CSP into the culture medium or introduction of the wild-type comC gene on a shuttle vector into the comCDE deletion mutant partially restored the wild-type biofilm architecture and further supported this idea. We conclude that the quorum-sensing signaling system essential for genetic competence in S. mutans is important for the formation of biofilms by this gram-positive organism.

Bacterial Proteins↗

PubMed2005

The Pseudomonas aeruginosa quorum-sensing molecule N-(3-oxododecanoyl)-L-homoserine lactone stimulates phagocytic activity in human macrophages through the p38 MAPK pathway.

Quorum-sensing is an important mechanism for the regulation of bacteria-to-bacteria communication. Recent advances have demonstrated that the Pseudomonas aeruginosa signaling molecule N-(3-oxododecanoyl)-L-homoserine lactone (3O-C(12)-HSL) is also a potent modulator of eukaryotic cells and may thus play an important role in the host response during P. aeruginosa infections. Little is known, however, about specific effects of 3O-C(12)-HSL molecules on human macrophages. To address this issue, we investigated the influence of 3O-C(12)-HSL on the phagocytic activity, production of reactive oxygen species, and activation of p38 and p42/44 MAPK signaling pathways in human macrophages. We show an effect of 3O-C(12)-HSL on the phagocytic capacity in human macrophages, which depends on concentration and time of exposure. When cells were exposed to 100 microM 3O-C(12)-HSL for 30 min or 1 h, the phagocytic activity increased 1.8 and 1.6 times, respectively. The 3O-C(12)-HSL treatments had no significant effect on the level of reactive oxygen species production. Furthermore, the p38 MAPK, but not the p42/44 MAPK, signaling pathway was activated in response to 3O-C(12)-HSL. In addition, specific blocking of p38 MAPK activation with 10 microM SB 203580 prevented the 3O-C(12)-HSL-induced increase in the phagocytic activity. These findings demonstrate that the bacterial quorum-sensing can play a significant role also in regulation of macrophage activity during infections caused by P. aeruginosa.

4-Butyrolactone↗

PubMed1998

Biofilms on indwelling urethral catheters produce quorum-sensing signal molecules in situ and in vitro.

Acylated homoserine lactones (AHLs) are chemical signals that mediate population density-dependent (quorum-sensing) gene expression in numerous gram-negative bacteria. In this study, gram-negative bacilli isolated from catheters were screened for AHL production by a cross-feeding assay utilizing an AHL-responsive Agrobacterium tumefaciens reporter strain. Positive reactions were obtained from 14 isolates of Pseudomonas aeruginosa; negative or weakly positive reactions were recorded for isolates of five other species. P. aeruginosa biofilms were then produced on catheters in a physical model of the bladder. Sections of colonized all-silicone catheters gave positive reactions for the quorum-sensing signal molecules as did sections that had been cleaned of biofilm and autoclaved. Control sections of unused catheters were negative in the tests. Sections from four of nine catheters that had been freshly removed from patients gave positive reactions for AHLs. Cleaned autoclaved sections of three of these catheters also gave strongly positive reactions for AHLs. These results demonstrate that AHLs are produced by biofilms as they develop on the catheters both in vitro in the model and in vivo in the patient's bladder. They represent the first demonstration of AHL production by biofilms in a clinical setting.

4-Butyrolactone↗

PubMed2006

Quorum-sensing inhibitors as anti-pathogenic drugs.

Quorum-sensing (QS) signalling systems of pathogens are central regulators for the expression of virulence factors and represent highly attractive targets for the development of novel therapeutics. In Pseudomonas aeruginosa, QS systems are also involved in elevated antibiotic tolerance of biofilms as well as elevated tolerance to the activity of the innate immune system. Gram-negative bacteria commonly use N-acyl homoserine lactones (AHL) as QS signal molecules. The use of signal molecule based drugs to attenuate bacterial pathogenecity rather than bacterial growth is attractive for several reasons, particularly considering the emergence of increasingly antibiotic-resistant bacteria. Compounds capable of this type of interference have been termed anti-pathogenic drugs. A large variety of synthetic AHL analogues and natural products libraries have been screened and a number of QS inhibitors (QSI) have been identified. Promising QSI compounds have been shown to make biofilms more susceptible to antimicrobial treatments, and are capable of reducing mortality and virulence as well as promoting clearance of bacteria in experimental animal models of infection.

4-Butyrolactone↗

PubMed2005

Degradation and synthesis kinetics of quorum-sensing autoinducer in Pseudomonas aeruginosa cultivation.

The quorum-sensing (las and rhl) systems play critical roles in the pathogenicity of Pseudomonas aeruginosa and its synthesis of the important biosurfactants, rhamnolipids. In this work, P. aeruginosa PAO1 and its rhlI and rhlR null mutants were used to study the degradation and synthesis kinetics of the rhl system's autoinducer PAI2 (N-butanoyl-homoserine lactone). The two mutants, lacking the ability of synthesizing PAI2 or RhlR protein, produced insignificant amounts of rhamnolipids while having similar growth profiles as the wild-type culture. The regulatory RhlR:PAI2 complex is thus essential to rhamnolipid synthesis. In batch culture of the wild-type PAO1, the autoinducer PAI2 concentration increased along cell growth, especially during the transition from exponential-growth phase to stationary phase, and began to decrease after entering the stationary phase. The decrease in the stationary phase resulted from a faster PAI2 degradation than its synthesis. The degradation kinetics was studied using PAI2-containing supernatants (from centrifuged broth of wild-type culture) with and without the rhlI(-) mutant cells incapable of PAI2 synthesis. Being insignificant in the cell-free systems, PAI2 degradation was found predominantly cell-associated and could be described empirically by the first-order, exponential decay kinetics with the best-fit degradation constant (k(d)) of 0.195 h(-1). When similarly modeled with a first-order kinetics, PAI2 synthesis in stationary-phase wild-type culture was derived to have a synthesis constant (k(s)) of 0.189 h(-1). The PAI2 concentration in batch cultivation of the rhlR(-) mutant also showed an increase-then-decrease profile. However, the maximum PAI2 concentration was about one third of that from the wild-type culture. The constitutive rate of PAI2 synthesis was therefore significantly lower than the rate attainable with active auto-induction by RhlR-PAI2 complex.

Aldose-Ketose Isomerases↗

PubMed2003

The alternative sigma factor RpoN regulates the quorum sensing gene rhlI in Pseudomonas aeruginosa.

The rhl quorum sensing (QS) circuit of Pseudomonas aeruginosa is known to regulate the expression of a number of virulence factors. This study investigates the regulation of rhlI, encoding the auto-inducer synthase RhlI responsible for the synthesis of N-butryl-L-homoserine lactone (BHL). A putative RpoN binding site was located upstream, in the promoter region of rhlI. Utilising a rhlI-lacZ transcriptional reporter, we demonstrate that under certain media conditions RpoN is a positive regulator of rhlI transcription. Measurements of BHL in extracted supernatant showed that the transcriptional patterns were reflected in the BHL levels, which were reduced in the rpoN mutant. Elastase and pyocyanin, known to be regulated by the rhl QS circuit, were shown to be reduced in a RpoN deficient strain. However, exogenous addition of BHL to the rpoN mutant did not restore these phenotypes suggesting that other regulatory factors apart from BHL are involved. Consistent with other rhl regulated phenotypes, we found that a rpoN mutant strain forms a biofilm that is different from that of the wild-type but similar to that displayed by a rhlI mutant.

Bacterial Proteins↗

PubMed2006

Hfq-dependent alterations of the transcriptome profile and effects on quorum sensing in Pseudomonas aeruginosa.

The Pseudomonas aeruginosa quorum-sensing (QS) systems, Las and Rhl, control the production of several virulence factors and other proteins, which are important to sustain adverse conditions. A comparative transcriptome analysis of a rpoS (-) and a rpoS(-)hfq( -) strain indicated that the Sm-like RNA-binding protein Hfq affects approximately 5% of the P. aeruginosa O1 transcripts. Among these transcripts 72 were identified to be QS regulated. Expression studies revealed that Hfq does not control the master regulators of the Las system, LasR and LasI. Upon entry into stationary phase, Hfq exerted a moderate stimulatory effect on translation of the rhlR gene and on the qscR gene, encoding a LasR/RhlR homologue. However, Hfq considerably stimulated translation of the rhlI gene, encoding the synthetase of the autoinducer N-Butyryl-homoserine lactone (C4-HSL). Correspondingly, the C4-HSL levels were reduced in a hfq(-) strain. To elucidate the stimulatory effect of Hfq on rhlI expression we asked whether Hfq affects the stability of the regulatory RNAs RsmY and RsmZ, which have been implicated in sequestration of the translational repressor RsmA, which in turn is known to negatively regulate RhlI synthesis. We demonstrate that Hfq binds to and stabilizes the regulatory RNA RsmY, which is further shown to bind to the regulatory protein RsmA. A model for the Hfq regulatory network is presented, wherein an alleviation of the negative effect of RsmA accounts for the observed stimulation of rhlI expression by Hfq. The model is corroborated by the observation that a rsmY(-) mutant mimics the hfq(-) phenotype with regard to rhlI expression.

Bacterial Proteins↗

PubMed2006

Type II quorum sensing regulates virulence in Erwinia carotovora ssp. carotovora.

Quorum sensing is a process by which bacteria communicate using secreted chemical signaling molecules called autoinducers. In this study, the opportunistic plant pathogen Erwinia carotovora ssp. carotovora was observed to secrete type II signaling molecules. A homolog of luxS, the gene required for AI-2 synthesis in Vibrio harveyi, was isolated from the genome of the pathogen. To determine the potential role of AI-2 in virulence, an isogenic luxS- (ECC) mutant was constructed and tested for its ability to cause tissue maceration. The findings reported here demonstrate that the LuxS-dependent signaling affects the progression of disease symptoms during the early stages of infection by modulating the expression of pectinolytic enzymes.

Bacterial Proteins↗

PubMed2006

PCR detection of Salmonella spp. using primers targeting the quorum sensing gene sdiA.

Bacteria communicate with one another and with their host using chemical signalling molecules. This phenomenon is generally described as quorum sensing. A set of primers for PCR detection of Salmonella spp. has been designed using as target the sdiA gene which encodes a signal receptor of the LuxR family. The PCR product (274 bp) was confirmed by sequencing. A number of 81 non-Salmonella strains (representing 24 different species) were tested and gave negative results, while a total of 101 different serotypes of Salmonella (155 strains) tested positive for the presence of the sdiA gene. The sensitivity and specificity of the sdiA-based PCR assay were also checked in artificially contaminated human faecal samples. In this study, we demonstrate that quorum sensing genes can be successfully exploited as diagnostic markers.

Animals↗

PubMed2005

Transcriptional autoregulation by quorum sensing Escherichia coli regulators B and C (QseBC) in enterohaemorrhagic E. coli (EHEC).

The cell-to-cell communication system referred to as quorum sensing (QS) is based on the principle that bacteria secrete hormone-like compounds referred to as autoinducers. Upon reaching a threshold concentration, these autoinducers interact with transcription factors to regulate gene expression. We previously reported that enterohaemorrhagic Escherichia coli (EHEC), which is responsible for outbreaks of bloody diarrhoea, utilizes a QS system to regulate gene transcription. We have also previously shown that the quorum sensing E. coli regulators B and C (QseBC) may act as a two-component system to transcriptionally regulate the expression of flagella and motility. Here, using a reverse transcription polymerase chain reaction (RT-PCR), we show that qseBC are transcribed in an operon. Furthermore, using a qseBC::lacZ transcriptional fusion, we observed that QseB autoactivates its own transcription. In addition, the transcriptional start site of the qseBC promoter responsive to QseBC was mapped, and single-copy and multicopy deletion analyses were performed to determine the minimal region necessary for QseB transcriptional activation. These data allowed us to map an additional transcriptional start site for the qseBC promoter which may allow for a basal level of QseBC expression. Finally, electrophoretic mobility shift assays, competition experiments and DNase I footprints were performed and demonstrated that QseB directly binds to two sites in its own promoter. These results indicate that QseB may act to autoregulate its own transcription through binding to low- and high-affinity sites found in its promoter.

Escherichia coli O157↗

PubMed2003

Role of the quorum-sensing system in experimental pneumonia due to Pseudomonas aeruginosa in rats.

The virulence of Pseudomonas aeruginosa is partly controlled by the las quorum-sensing system. A rat model of acute pneumonia was used to investigate the pathophysiological impact of this system by comparing the virulence of the wild-type virulent laboratory strain PAO1 with that of its lasR-deleted mutant PAOR. In comparison with PAO1, PAOR was avirulent after an instillation of 106 cfu (mortality rates, 72 versus 0%, respectively; p < 0.0001). A ten-fold higher inoculum slightly increased the mortality rate induced by PAOR (25%), which remained lower than that induced by PAO1 (75%, p = 0.0001). In addition, with both inocula lung and bronchoalveolar lavage bacterial counts were significantly lower in rats infected with PAOR than with PAO1 (p </= 0.01). Histopathological analysis showed that PAO1 induced a drastic vascular congestion and neutrophil infiltration of the lungs, whereas lung injury in rats infected with PAOR was mild with predominantly macrophage infiltration. This study adds evidence that the quorum-sensing system has an important role in the pathophysiology of P. aeruginosa pulmonary infection.

Animals↗