Quorum Sensing Mutants Research Articles

Bacterial Quorum Sensing During Infection.

Bacteria are highly interactive and possess an extraordinary repertoire of intercellular communication and social behaviors, including quorum sensing (QS). QS has been studied in detail at the molecular level, so mechanistic details are well understood in many species and are often involved in virulence. The use of different animal host models has demonstrated QS-dependent control of virulence determinants and virulence in several human pathogenic bacteria. QS also controls virulence in several plant pathogenic species. Despite the role QS plays in virulence during animal and plant laboratory-engineered infections, QS mutants are frequently isolated from natural infections, demonstrating that the function of QS during infection and its role in pathogenesis remain poorly understood and are fruitful areas for future research. We discuss the role of QS during infection in various organisms and highlight approaches to better understand QS during human infection. This is an important consideration in an era of growing antimicrobial resistance, when we are looking for new ways to target bacterial infections.

A Unique Combination of Two Different Quorum Sensing Systems in the β-Rhizobium Cupriavidus taiwanensis.

Cupriavidus taiwanensis LMG19424, a β-rhizobial symbiont of Mimosa pudica, harbors phc and tqs quorum sensing (QS), which are the homologous cell-cell communication systems previously identified from the plant pathogen Ralstonia solanacearum and the human pathogen Vibrio cholerae, respectively. However, there has been no experimental evidence reported that these QS systems function in C. taiwanensis LMG19424. We identified (R)-methyl 3-hydroxymyristate (3-OH MAME) and (S)-3-hydroxypentadecan-4-one (C15-AHK) as phc and tqs QS signals, respectively, and characterized these QS systems. The expression of the signal synthase gene phcB and tqsA in E. coli BL21(DE3) resulted in the high production of 3-OH MAME and C15-AHK, respectively. Their structures were elucidated by comparison of EI-MS data and GC/chiral LC retention times with synthetic standards. The deletion of phcB reduced cell motility and increased biofilm formation, and the double deletion of phcB/tqsA caused the accumulation of the metal chelator coproporphyrin III in its mutant culture. Although the deletion of phcB and tqsA slightly reduced its ability to nodulate on aseptically grown seedlings of M. pudica, there was no significant difference in nodule formation between LMG19424 and its QS mutants when commercial soils were used. Taken together, this is the first example of the simultaneous production of 3-OH MAME/C15-AHK as QS signals in a bacterial species, and the importance of the phc/tqs QS systems in the saprophytic stage of C. taiwanensis LMG19424 is suggested.

Disappearance of Quorum Sensing in Burkholderia glumae During Experimental Evolution.

The plant pathogen Burkholderia glumae uses quorum sensing (QS) that allows bacteria to share information and alter gene expression on the basis of cell density. The wild-type strain of B. glumae produces quorum-sensing signals (autoinducers) to detect their community and upregulate QS-dependent genes across the population for performing social and group behaviors. The model organism B. glumae was selected to investigate adaptation, estimate evolutionary parameters, and test diverse evolutionary hypotheses by using experimental evolution. The wild-type B. glumae virulent strain showed genotypic changes during regular subculture due to oxygen limitation. The laboratory-evolved clones failed to produce the signaling molecule of C8-HSL/C6-HSL for activation of the quorum-sensing system. Further, the laboratory-evolved clones failed to produce catalase and oxalate for protecting themselves from the toxic environment at stationary phase and phytotoxins (toxoflavin) for infecting rice grain, respectively. The laboratory-evolved clones were completely sequenced and compared with the wild-type. Sequencing analysis of the evolved clones revealed that mutations in QS-responsible genes (iclR), sensor genes (shk, mcp), and signaling genes (luxR) were responsible for quorum-sensing activity failure. The experimental results and sequencing analysis revealed quorum-sensing process failure in the laboratory-evolved clones. In conclusion, the wild-type B. glumae strain was often exposed to oxidative stress during regular subculture and evolved as an avirulent strain (quorum-sensing mutant) by losing the phenotypic and genotypic characteristics.

Quorum sensing-dependent post-secretional activation of extracellular proteases in Pseudomonas aeruginosa

Pseudomonas aeruginosa secretes multiple proteases that are implicated in its pathogenesis, and most of them are regulated by quorum sensing (QS). In this study, we found that the activities of three major extracellular proteases, protease IV (PIV), elastase A (LasA), and elastase B (LasB), are reduced considerably when expressed in a QS mutant (MW1). PIV and LasA expressed in MW1 exhibited little activity, even when purified, and their activities were inhibited by noncleavage or binding of their propeptides. LasB was activated by a QS-dependent factor, indicating that, unlike what has been proposed previously, LasB is not autoactivated. When LasB was relieved from inhibition, it activated PIV, which then sequentially processed pro-LasA to mature LasA. When activated, LasB was not inhibited by exogenous addition of its propeptide, but LasA and PIV were inhibited by their propeptides, even after prior activation. These differences may be explained by the fact that LasB can degrade its own propeptide but PIV and LasA cannot. We also found that, although PIV is the preferred LasA-activating factor, LasB can also partially activate LasA. Overall, LasB, PIV, and LasA were activated postsecretionally in a cascading manner in which the initial activation of LasB was controlled tightly by QS at the protein level in addition to the well-known transcriptional control of these proteases by QS. Interestingly, human elastase also activated LasA, indicating that the activation cascade is triggered by host factors during infection. In summary, a QS-induced proteolytic cascade activates secreted proteases from P. aeruginosa.

New insight into bacterial social communication in natural host: Evidence for interplay of heterogeneous and unison quorum response.

Many microbes exhibit quorum sensing (QS) to cooperate, share and perform a social task in unison. Recent studies have shown the emergence of reversible phenotypic heterogeneity in the QS-responding pathogenic microbial population under laboratory conditions as a possible bet-hedging survival strategy. However, very little is known about the dynamics of QS-response and the nature of phenotypic heterogeneity in an actual host-pathogen interaction environment. Here, we investigated the dynamics of QS-response of a Gram-negative phytopathogen Xanthomonas pv. campestris (Xcc) inside its natural host cabbage, that communicate through a fatty acid signal molecule called DSF (diffusible signal factor) for coordination of several social traits including virulence functions. In this study, we engineered a novel DSF responsive whole-cell QS dual-bioreporter to measure the DSF mediated QS-response in Xcc at the single cell level inside its natural host plant in vivo. Employing the dual-bioreporter strain of Xcc, we show that QS non-responsive cells coexist with responsive cells in microcolonies at the early stage of the disease; whereas in the late stages, the QS-response is more homogeneous as the QS non-responders exhibit reduced fitness and are out competed by the wild-type. Furthermore, using the wild-type Xcc and its QS mutants in single and mixed infection studies, we show that QS mutants get benefit to some extend at the early stage of disease and contribute to localized colonization. However, the QS-responding cells contribute to spread along xylem vessel. These results contrast with the earlier studies describing that expected cross-induction and cooperative sharing at high cell density in vivo may lead to synchronize QS-response. Our findings suggest that the transition from heterogeneity to homogeneity in QS-response within a bacterial population contributes to its overall virulence efficiency to cause disease in the host plant under natural environment.

Dynamics of cheater invasion in a cooperating population of Pseudomonas aeruginosa

Pseudomonas aeruginosa quorum sensing (QS) regulates expression of dozens of genes in a cell density-dependent manner. Many QS-regulated genes code for production of extracellular factors, “public goods” that can benefit the entire population. This cooperation encourages individuals to cheat by using but not producing public goods. QS also controls expression of a limited number of genes encoding “private” cellular enzymes like Nuh, an enzyme involved in adenosine catabolism. Growth of P. aeruginosa on casein requires QS-regulated production of an extracellular protease and is an example of cooperative behavior. When P. aeruginosa is transferred daily on casein, QS mutants emerge. These cheaters have mutations in lasR, which encodes the primary QS transcription factor. When growth is on casein and adenosine, cheater emergence is constrained. Here, we report the dynamics of LasR mutant invasion during growth on casein or casein plus adenosine. We show that LasR mutants have the greatest advantage during early to mid-logarithmic growth on casein. Addition of adenosine to casein medium constrains cheaters throughout growth. Our data support the view that co-regulation of the public protease and the private nucleosidase by QS stabilizes cooperation, and the data are not consistent with other proposed alternate hypotheses.

Differential effects of alkyl gallates on quorum sensing in Pseudomonas aeruginosa

Virulence factors and biofilms constitute attractive targets for the prevention of infections caused by multidrug-resistant bacteria. Among alkyl gallates, propyl gallate (PG) and octyl gallate (OG) are used as food preservatives. Here we found that alkyl gallates differentially affect virulence, biofilm formation, and quorum sensing (QS) in Pseudomonas aeruginosa. Ethyl gallate (EG), PG, and butyl gallate (BG) inhibited biofilm formation and virulence factors including elastase, pyocyanin, and rhamnolipid, in P. aeruginosa without affecting cell viability by antagonizing the QS receptors LasR and RhlR. PG exhibited the most potent activity. Interestingly, hexyl gallate (HG) inhibited the production of rhamnolipid and pyocyanin but did not affect elastase production or biofilm formation. Notably, OG inhibited the production of rhamnolipid and pyocyanin but stimulated elastase production and biofilm formation. Analysis of QS signaling molecule production and QS gene expression suggested that HG inhibited RhlR, while OG activated LasR but inhibited PqsR. This mechanism was confirmed using QS mutants. Additionally, PG prevented the virulence of P. aeruginosa in Caenorhabditis elegans and a mouse model. This is the first report of the differential effects of alkyl gallates on QS systems and PG has great potential as an inhibitor of the virulence and biofilm formation of P. aeruginosa.

Resistance to leukocytes ties benefits of quorum sensing dysfunctionality to biofilm infection.

Social interactions play an increasingly recognized key role in bacterial physiology1. One of the best studied is quorum sensing (QS), a mechanism by which bacteria sense and respond to the status of cell density2. While QS is generally deemed crucial for bacterial survival, QS-dysfunctional mutants frequently arise in in-vitro culture. This has been explained by the fitness cost an individual mutant, a “quorum cheater”, saves at the expense of the community3. QS mutants are also often isolated from biofilm-associated infections, including cystic fibrosis lung infection4, as well as medical device infection and associated bacteremia5–7. However, despite the frequently proposed use of QS blockers to control virulence8, the mechanisms underlying QS dysfunctionality during infection have remained poorly understood. Here we show that in the major human pathogen Staphylococcus aureus, QS-dysfunctional mutants arise exclusively in biofilm infection, while in non-biofilm-associated infection there is a high selective pressure to maintain QS control. We demonstrate that this infection-type dependence is due to QS-dysfunctional bacteria having a significant survival advantage in biofilm infection, because they form dense and enlarged biofilms that provide resistance to phagocyte attacks. Our results link the benefit of QS-dysfunctional mutants in vivo to biofilm-mediated immune evasion, thus to mechanisms that are specific to the in-vivo setting. Notably, our findings explain why QS mutants are frequently isolated from biofilm-associated infections and provide guidance for the therapeutic application of QS blockers.

Quorum sensing is required for full virulence of Vibrio campbellii towards tiger grouper (Epinephelus fuscoguttatus) larvae.

The link between quorum sensing in Vibrio campbellii and its virulence towards tiger grouper (Epinephelus fuscoguttatus) was investigated using V. campbellii wild type and quorum-sensing mutants with inactive quorum sensing or constitutively maximal quorum-sensing activity, and signal molecule synthase mutants. The results showed that wild-type V. campbellii is pathogenic to grouper larvae, causing more than 50% mortality after 4days of challenge. Furthermore, the mortality of larvae challenged with the mutant with maximally active quorum sensing was significantly higher than that of larvae challenged with the wild type, whereas a higher survival was observed in the larvae challenged to the mutant with a completely inactive quorum-sensing system. Grouper larvae challenged with either the signal molecule synthase triple mutant, the harveyi autoinducer-1 (HAI-1) synthase mutant and the autoinducer-2 (AI-2) synthase mutant showed higher survival than larvae challenged with the wild type. In contrast, larvae challenged with the cholerae autoinducer-1 (CAI-1) synthase mutant showed high mortality. This indicates that HAI-1 and AI-2, but not CAI-1, are required for full virulence of V.campbellii towards grouper larvae. Our data suggest that quorum-sensing inhibition could be an effective strategy to control V. campbellii infections in tiger grouper.

Terrein is an inhibitor of quorum sensing and c-di-GMP in Pseudomonas aeruginosa: a connection between quorum sensing and c-di-GMP

To address the drug-resistance of bacterial pathogens without imposing a selective survival pressure, virulence and biofilms are highly attractive targets. Here, we show that terrein, which was isolated from Aspergillus terreus, reduced virulence factors (elastase, pyocyanin, and rhamnolipid) and biofilm formation via antagonizing quorum sensing (QS) receptors without affecting Pseudomonas aeruginosa cell growth. Additionally, the effects of terrein on the production of QS signaling molecules and expression of QS-related genes were verified. Interestingly, terrein also reduced intracellular 3,5-cyclic diguanylic acid (c-di-GMP) levels by decreasing the activity of a diguanylate cyclase (DGC). Importantly, the inhibition of c-di-GMP levels by terrein was reversed by exogenous QS ligands, suggesting a regulation of c-di-GMP levels by QS; this regulation was confirmed using P. aeruginosa QS mutants. This is the first report to demonstrate a connection between QS signaling and c-di-GMP metabolism in P. aeruginosa, and terrein was identified as the first dual inhibitor of QS and c-di-GMP signaling.

A simple mung bean infection model for studying the virulence of Pseudomonas aeruginosa.

Here we highlight the development of a simple and high-throughput mung bean model to study virulence in the opportunistic pathogen Pseudomonas aeruginosa. The model is easy to set up, and infection and virulence can be monitored for up to 10 days. In a first test of the model, we found that mung bean seedlings infected with PAO1 showed poor development of roots and high mortality rates compared to uninfected controls. We also found that a quorum-sensing (QS) mutant was significantly less virulent when compared with the PAO1 wild-type. Our work introduces a new tool for studying virulence in P. aeruginosa that will allow for high-throughput virulence studies of mutants and testing of the in vivo efficacy of new therapies at a time when new antimicrobial drugs are desperately needed.

Transcriptome Profiling Reveals the EanI/R Quorum Sensing Regulon in Pantoea Ananatis LMG 2665T.

Pantoea ananatis LMG 2665T synthesizes and utilizes acyl homoserine lactones (AHLs) for signalling. The complete set of genes regulated by the EanI/R quorum sensing (QS) system in this strain is still not fully known. In this study, RNA-sequencing (RNA-seq) was used to identify the EanI/R regulon in LMG 2665T. Pairwise comparisons of LMG 2665T in the absence of AHLs (Optical density (OD)600 = 0.2) and in the presence of AHLs (OD600 = 0.5) were performed. Additionally, pairwise comparisons of LMG 2665T and its QS mutant at OD600 = 0.5 were undertaken. In total, 608 genes were differentially expressed between LMG 2665T at OD600 = 0.5 versus the same strain at OD600 = 0.2 and 701 genes were differentially expressed between LMG 2665T versus its QS mutant at OD600 = 0.5. A total of 196 genes were commonly differentially expressed between the two approaches. These constituted approximately 4.5% of the whole transcriptome under the experimental conditions used in this study. The RNA-seq data was validated by reverse transcriptase quantitative polymerase chain reaction (RT-qPCR). Genes found to be regulated by EanI/R QS were those coding for redox sensing, metabolism, flagella formation, flagella dependent motility, cell adhesion, biofilm formation, regulators, transport, chemotaxis, methyl accepting proteins, membrane proteins, cell wall synthesis, stress response and a large number of hypothetical proteins. The results of this study give insight into the genes that are regulated by the EanI/R system in LMG 2665T. Functional characterization of the QS regulated genes in LMG 2665T could assist in the formulation of control strategies for this plant pathogen.

Nitrogen Source Stabilization of Quorum Sensing in the Pseudomonas aeruginosa Bioaugmentation Strain SD-1.

Pseudomonas aeruginosa SD-1 is efficient at degrading aromatic compounds and can therefore contribute to the bioremediation of wastewater. P. aeruginosa uses quorum sensing (QS) to regulate the production of numerous secreted "public goods." In wastewater bioaugmentation applications, there are myriad nitrogen sources, and we queried whether various nitrogen sources impact the stabilities of both QS and the bacterial populations. In a laboratory strain of P. aeruginosa, PAO1, the absence of a nitrogen source has been shown to destabilize these populations through the emergence of QS mutant "cheaters." We tested the ability of SD-1 to grow in casein broth, a condition that requires QS for growth, when the nitrogen source with either NH4Cl, NaNO3, or NaNO2 or with no added nitrogen source. There was great variability in susceptibility to invasion by QS mutant cheaters and, by extension, the stability of the SD-1 population. When grown with NH4Cl as an extra nitrogen source, no population collapse was observed; by contrast, two-thirds of cultures grown in the presence of NaNO2 collapsed. In the populations that collapsed, the frequency of social cheaters exceeded 40%. NaNO3 and NaNO2 directly favor QS mutants of P. aeruginosa SD-1. Although the mechanism by which these nitrogen sources act is not clear, these data indicate that the metabolism of nitrogen can affect the stability of bacterial populations, an important observation for continuing industrial applications with this species.IMPORTANCE Bioaugmentation as a method to help remediate wastewater pollutant streams holds significant potential to enhance traditional methods of treatment. Addition of microbes that can catabolize organic pollutants can be an effective method to remove several toxic compounds. Such bioaugmented strains of bacteria have been shown to be susceptible to competition from the microbiota that are present in wastewater streams, limiting their potential effectiveness. Here, we show that bioaugmentation strains of bacteria might also be susceptible to invasion by social cheaters and that the nitrogen sources available in the wastewater might influence the ability of cheaters to overtake the bioaugmentation strains. Our results imply that control over the nitrogen sources in a wastewater stream or selective addition of certain nitrogen sources could help stabilize bioaugmentation strains of bacteria.

Post-secretional activation of Protease IV by quorum sensing in Pseudomonas aeruginosa

Protease IV (PIV), a key virulence factor of Pseudomonas aeruginosa is a secreted lysyl-endopeptidase whose expression is induced by quorum sensing (QS). We found that PIV expressed in QS mutant has severe reduction of activity in culture supernatant (CS), even though it is overexpressed to high level. PIV purified from the QS mutant (M-PIV) had much lower activity than the PIV purified from wild type (P-PIV). We found that the propeptide cleaved from prepro-PIV was co-purified with M-PIV, but never with P-PIV. Since the activity of M-PIV was restored by adding the CS of QS-positive and PIV-deficient strain, we hypothesized that the propeptide binds to and inhibits PIV, and is degraded to activate PIV by a QS-dependent factor. In fact, the CS of the QS-positive and PIV-deficient strain was able to degrade the propeptide. Since the responsible factor should be a QS-dependently expressed extracellular protease, we tested QS-dependent proteases of P. aeruginosa and found that LasB (elastase) can degrade the propeptide and activate M-PIV. We purified the propeptide of PIV and confirmed that the propeptide can bind to and inhibit PIV. We suggest that PIV is post-secretionally activated through the extracellular degradation of the propeptide by LasB, a QS-dependent protease.

Critical role of quorum sensing-dependent glutamate metabolism in homeostatic osmolality and outer membrane vesiculation in Burkholderia glumae

Metabolic homeostasis in cooperative bacteria is achieved by modulating primary metabolism in a quorum sensing (QS)-dependent manner. A perturbed metabolism in QS mutants causes physiological stress in the rice bacterial pathogen Burkholderia glumae. Here, we show that increased bacterial osmolality in B. glumae is caused by unusually high cellular concentrations of glutamate and betaine generated by QS deficiencies. QS negatively controls glutamate uptake and the expression of genes involved in the glutamine synthetase and glutamine oxoglutarate aminotransferase cycles. Thus, cellular glutamate levels were significantly higher in the QS mutants than in the wild type, and they caused hyperosmotic cellular conditions. Under the hypotonic conditions of the periplasm in the QS mutants, outer membrane bulging and vesiculation were observed, although these changes were rescued by knocking out the gltI gene, which encodes a glutamate transporter. Outer membrane modifications were not detected in the wild type. These results suggest that QS-dependent glutamate metabolism is critical for homeostatic osmolality. We suggest that outer membrane bulging and vesiculation might be the outcome of a physiological adaptation to relieve hypotonic osmotic stress in QS mutants. Our findings reveal how QS functions to maintain bacterial osmolality in a cooperative population.

Response of Salmonella Typhi to bile-generated oxidative stress: implication of quorum sensing and persister cell populations.

Salmonella Typhi can chronically persist within the gallbladder of patients suffering from gallbladder diseases. This study, intended to improve our understanding of bacterial mechanisms underlying bile adaptation, revealed that bile, which is a bactericidal agent, led to the generation of reactive oxygen species in S Typhi. Salmonella Typhi in response showed a significant increase in the production of anti-oxidative enzymes, namely superoxide dismutase and catalase. The work reports that the quorum-sensing (QS) system of S Typhi regulates the level of these enzymes during oxidative stress. In support of these observations, the quorum-sensing mutant of S Typhi was found to be sensitive to bile with significantly lower levels of anti-oxidant enzymes compared to other clinical isolates. Furthermore the addition of exogenous cell-free extracts (CFEs) of S Typhi containing the quorum-sensing signalling molecule significantly increased the levels of these enzymes within the mutant. Interestingly the CFE addition did not significantly restore the biofilm-forming ability of the mutant strain when compared with the wild-type. In the presence of ciprofloxacin and ampicillin, S Typhi formed persister cells which increased >3-fold in the presence of bile. Thus the QS-system of S Typhi aids in oxidative stress management, and enhanced persister cell populations could assist chronic bacterial persistence within the gallbladder.

Quorum sensing is crucial to Escherichia coli O157:H7 biofilm formation under static or very slow laminar flow conditions

Quorum sensing (QS) is defined as a cellto- cell signaling process that collectively regulates the gene expression of bacteria via small signaling molecules called autoinducers (AIs). It was reported that QS-regulated gene expression in Pseudomonas aeruginosa failed to occur at a high Reynolds number (Re= 3,000), since AI-2, a secreted interspecies signaling molecule, was washed away and so could not reach the minimum concentration required for QS. In this study, we describe the effects of flow speed on QS-stimulated biofilm formation in Escherichia coli O157:H7 inside a very thin microchannel (3 cm×1 cm×45 μm). In microtiter plates, the wild-type strain produced high amounts of exopolysaccharide, whereas its QS mutants ΔluxS and ΔlsrK, defective in AI-2 production and phosphorylation, made less exopolysaccharide. Confocal laser scanning microscopy showed that at a flow rate of 1 μL/min the wild-type strain formed rounded biofilms, whereas such biofilms formed by the QS mutants were fewer and thinner. At a flow rate of 10 μL/min, none of the tested strains formed mature biofilms. Our results suggest that QS is essential in the biofilm maturation under static or very slow laminar flow conditions where the biofilm signal can be easily accumulated and transported to the sessile cells.

Bacterial Quorum Sensing Stabilizes Cooperation by Optimizing Growth Strategies.

Cooperation is a fundamental problem for evolutionary biology to explain. Conditional participation through phenotypic plasticity driven by communication is a potential solution to this dilemma. Thus, among bacteria, QS has been proposed to be a proximate stabilizing mechanism for cooperative behaviors. Here, we empirically demonstrate that QS in V. harveyi prevents cheating and subsequent invasion by nonproducing defectors by maximizing the growth rate at low cell densities and the growth yield at high cell densities, whereas an unconditional cooperator is rapidly driven to extinction by defectors. Our findings provide experimental evidence that QS regulation prevents the invasion of cooperative populations by QS defectors even under unstructured conditions, and they strongly support the role of communication in bacteria as a mechanism that stabilizes cooperative traits.

Quorum sensing control of Type VI secretion factors restricts the proliferation of quorum-sensing mutants.

Burkholderia thailandensis uses acyl-homoserine lactone-mediated quorum sensing systems to regulate hundreds of genes. Here we show that cell-cell contact-dependent type VI secretion (T6S) toxin-immunity systems are among those activated by quorum sensing in B. thailandensis. We also demonstrate that T6S is required to constrain proliferation of quorum sensing mutants in colony cocultures of a BtaR1 quorum-sensing signal receptor mutant and its parent. However, the BtaR1 mutant is not constrained by and outcompetes its parent in broth coculture, presumably because no cell contact occurs and there is a metabolic cost associated with quorum sensing gene activation. The increased fitness of the wild type over the BtaR1 mutant during agar surface growth is dependent on an intact T6SS-1 apparatus. Thus, quorum sensing activates B. thailandensis T6SS-1 growth inhibition and this control serves to police and constrain quorum-sensing mutants. This work defines a novel role for T6SSs in intraspecies mutant control.

Curcumin from Curcuma longa affects the virulence of Pectobacterium wasabiae and P. carotovorum subsp. carotovorum via quorum sensing regulation

In plant soft-rotting bacteria Pectobacterium, quorum sensing (QS) regulates the secretion of an arsenal of plant cell wall degrading extracellular enzymes (PCWDEs) and flagella-mediated motility via two different signaling molecules such as 3-oxohexanoyl-L-homoserine lactone (3-oxo-C6-AHL) and 3-oxooctanoyl-L-homoserine lactone (3-oxo- C8-AHL). In the present investigation, the phytochemical compound curcumin was assessed for its QS inhibitory potential against AHL-dependent PCWDEs production and motility in P. wasabiae SCC3193, P. carotovorum subsp. Carotovorum Pcc21 and P. carotovorum subsp. Carotovorum Pcc. Interestingly, curcumin at sub-MIC effectively inhibited the production of PCWDEs as well as the swimming and swarming motility of all tested pathogens in a non-bactericidal fashion. Subsequently, the in vitro root pathogenicity assay in Arabidopsis thaliana unveiled the rescuing efficacy of curcumin against the pathogenicity of tested plant pathogens by attenuating its QS mediated virulence factors production. Besides, studies with QS mutant strain Pcc21-M10 also evidenced the QSI property of curcumin.