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    The production of bacterial cellulose in Gluconacetobacter xylinus regulated by luxR overexpression of quorum sensing system
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    Quorum sensing (QS) is a communication procedure that predominates gene expression in response to cell density and fluctuations in the neighboring environment as a result of discerning molecules termed autoinducers (AIs). It has been embroiled that QS can govern bacterial behaviors such as the secretion of virulence factors, biofilm formation, bioluminescence production, conjugation, sporulation and swarming motility. Autoinducer 2 (AI-2), a QS signaling molecule brought up to be involved in interspecies communication, exists in both gram-negative and -positive bacteria. Therefore, novel approaches to interrupt AI-2 quorum sensing are being recognized as next generation antimicrobials. In the present review article, we summarized recent progresses on AI-2 bacterial quorum sensing inhibitors and discussed their potential as the antibacterial agents. Keywords: AI-2, bacteria, inhibitors, LuxP, LuxS, quorum sensing, bioluminescence, predominates gene expression, antibacterial agents, autoinducers
    Autoinducer
    Swarming motility
    Cell Signaling
    Citations (35)
    Quorum sensing is the regulation of gene expression in response to fluctuations in cell-population density. Quorum sensing bacteria produce and release chemical signal molecules called autoinducers that increase in concentration as a function of cell density. The detection of a minimal threshold stimulatory concentration of an autoinducer leads to an alteration in gene expression. Gram-positive and Gram-negative bacteria use quorum sensing communication circuits to regulate a diverse array of physiological activities. These processes include symbiosis, virulence, competence, conjugation, antibiotic production, motility, sporulation, and biofilm formation. In general, Gram-negative bacteria use acylated homoserine lactones as autoinducers, and Gram-positive bacteria use processed oligo-peptides to communicate. Recent advances in the field indicate that cell-cell communication via autoinducers occurs both within and between bacterial species. Furthermore, there is mounting data suggesting that bacterial autoinducers elicit specific responses from host organisms. Although the nature of the chemical signals, the signal relay mechanisms, and the target genes controlled by bacterial quorum sensing systems differ, in every case the ability to communicate with one another allows bacteria to coordinate the gene expression, and therefore the behavior, of the entire community. Presumably, this process bestows upon bacteria some of the qualities of higher organisms. The evolution of quorum sensing systems in bacteria could, therefore, have been one of the early steps in the development of multicellularity.
    Autoinducer
    Homoserine
    Citations (4,779)
    Bacteria monitor their local population densities using small molecules (or autoinducers) in a process known as quorum sensing. Here, we report a new and efficient synthetic route to naturally occurring bacterial autoinducers [N-acyl l-homoserine lactones (AHLs)] that is readily amenable to the synthesis of analogues. This route has been applied in the first synthesis of a library of non-native AHLs. Evaluation of these compounds in bacterial reporter gene and biofilm assays has revealed a potent set of quorum sensing antagonists. These ligands will serve as valuable new tools to explore the role of quorum sensing in bacterial pathogenesis.
    Autoinducer
    Homoserine
    Citations (300)
    Communication among bacteria with quorum-sensing system is accomplished through the exchange of signal molecules called autoinducers.When the densities of autoinducers rise to a certain degree,bacteria respond by specialized gene expression such as biofilm,bioluminescence,virulence and sporulation.Recently many quorum sensing inhibitors,which specifically interfere with the QS circuit,were discovered or synthesized. Detailed review regarding the autoinducer,inhibitors,significance and prospect of bacterial quorum-sensing system has been presented in this paper.
    Autoinducer
    Citations (1)
    According to the cell density bacteria can regulate their gene expression. Gene regulation is initiated by the release of signaling molecules into the environment which are called autoinducers. When the population density increases, these autoinducers accumulate extracellularly and these can be detected by the bacteria through quorum sensing. We found that E. coli make use of indole quorum-sensing signals to prevent it from infection by T4 phage. This has been acknowledged for the first time that E. coli utilizes antiphage defense mechanism regulated by quorum sensing. We proposed that through quorum sensing E. coli is protected in conditions where there is increased risk of infection as for example during growth in high cellular density in which there is mixed species environments. In microbial communities, quorum-sensing is a general phenomenon which controls E. coli susceptibility to phage.
    Autoinducer
    Cell Signaling
    Citations (2)
    Quorum sensing is a bacterial cell to cell communication, which helps bacteria to mount population-density-dependent infection to overcome the defence responses from the host. In this mechanism some diffusible chemical signalling compounds are involved, known as autoinducers, which are directly proportional to the population cell density. The main role of quorum sensing is to coordinate the expression of several collective traits, including biofilm formation, bioluminescence, epiphytic fitness, Production of virulence factors, secondary metabolites with antimicrobial activity, pigments, siderophores, plasmid transfer and motility. Due to the growing bacterial resistance to the antibiotics that have been overused, it has become necessary to search for alternative antimicrobial therapies. One of them is anti-quorum sensing agents/anti-biofilm agents/quorum sensing inhibitors that disrupts the bacterial communication. This review article discusses the various quorum sensing-disrupting mechanisms used by anti-quorum sensing agents such as, inhibition of Autoinducer synthesis inhibition of transport of Autoinducers, degradation of autoinducers using enzymes, sequestration using monoclonal antibodies, signal competition, as well as the different techniques applied artificially to inhibit the quorum sensing pathways in bacteria and thus, protecting plant from bacterial diseases.
    Autoinducer
    Bioreporter
    Many Gram-negative bacteria communicate via molecules called autoinducers to coordinate the activities of their populations. Such communication is termed quorum sensing and can regulate pathogenic virulence factor production and antimicrobial resistance. The quorum sensing system of Pseudomonas aeruginosa is currently the most intensively researched, because this bacterium is an opportunistic human pathogen annually responsible for the death of thousands of cystic fibrosis sufferers and many other immunocompromised individuals. Quorum sensing inhibitors can attenuate the pathogenicity of P. aeruginosa. Here we present the crystal structure of the P. aeruginosa LasR ligand-binding domain bound to its autoinducer 3-oxo-C(12)-acylhomoserine lactone. The structure is a symmetrical dimer, with each monomer exhibiting an alpha-beta-alpha fold similar to the TraR and SdiA quorum sensing proteins of Agrobacterium tumefaciens and Escherichia coli. The structure was determined up to 1.8-A resolution and reveals the atomic interactions between LasR and its autoinducer. The monomer structures of LasR, TraR, and SdiA are comparable but display differences in their quaternary organization. Inspection of their binding sites shows some unexpected variations resulting in quite different conformations of their bound autoinducers. We modeled interactions between LasR and various quorum sensing inhibitors, yielding insight into their possible mechanisms of action. The structure also provides a platform for the optimization, or de novo design, of quorum sensing inhibitors.
    Autoinducer
    Virulence factor
    Human pathogen
    Citations (393)
    ABSTRACT We report that 2 μg of azithromycin/ml inhibits the quorum-sensing circuitry of Pseudomonas aeruginosa strain PAO1. Addition of synthetic autoinducers partially restored the expression of the trancriptional activator-encoding genes lasR and rhlR but not that of the autoinducer synthase-encoding gene lasI . We propose that azithromycin interferes with the synthesis of autoinducers, by an unknown mechanism, leading to a reduction of virulence factor production.
    Autoinducer
    Homoserine