Quorum sensing in Vibrio harveyi: probing the specificity of the LuxP binding site

Lowery, Colin A.; McKenzie, Kathleen M.; Qi, Longwu; Meijler, Michaël M.; Janda, Kim D.

doi:10.1016/j.bmcl.2005.02.069

Cited by 45 publications

(35 citation statements)

References 19 publications

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“…(5) Hospital Sao Paulo Salmonella sp. (1) Hospital Sao Paulo K. pneumoniae (17) Hospital Sao Paulo E. cloacae (1) Hospital Sao Paulo Citrobacter diversus (1) Hospital Sao Paulo In vitro synthesis of AI-2. In vitro synthesis of AI-2 was carried out as previously described (30).…”

Section: Methodsmentioning

confidence: 99%

“…harveyi bioluminescence assay. AI-2 activity in preconditioned (PC) medium, enzymatically derived AI-2, and chemically synthesized DPD AI-2 precursor (a gift from Michael Meijler and Kim D. Janda, The Scripps Research Institute) (17) was assayed by using the V. harveyi BB170 reporter strain, which responds only to AI-2 (17,37). The assays were performed as previously described (37) and read using a Bio-Rad Lumimark microplate reader.…”

Section: Methodsmentioning

confidence: 99%

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AI-3 Synthesis Is Not Dependent onluxSinEscherichia coli

2006

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The quorum-sensing (QS) signal autoinducer-2 (AI-2) has been proposed to promote interspecies signaling in a broad range of bacterial species. AI-2 is spontaneously derived from 4,5-dihydroxy-2,3-pentanedione that, along with homocysteine, is produced by cleavage of S-adenosylhomocysteine (SAH) and S-ribosylhomocysteine by the Pfs and LuxS enzymes. Numerous phenotypes have been attributed to AI-2 QS signaling using luxS mutants. We have previously reported that the luxS mutation also affects the synthesis of the AI-3 autoinducer that activates enterohemorrhagic Escherichia coli virulence genes. Here we show that several species of bacteria synthesize AI-3, suggesting a possible role in interspecies bacterial communication. The luxS mutation leaves the cell with only one pathway, involving oxaloacetate and L-glutamate, for de novo synthesis of homocysteine. The exclusive use of this pathway for homocysteine production appears to alter metabolism in the luxS mutant, leading to decreased levels of AI-3. The addition of aspartate and expression of an aromatic amino acid transporter, as well as a tyrosine-specific transporter, restored AI-3-dependent phenotypes in an luxS mutant. The defect in AI-3 production, but not in AI-2 production, in the luxS mutant was restored by expressing the Pseudomonas aeruginosa S-adenosylhomocysteine hydrolase that synthesizes homocysteine directly from SAH. Furthermore, phenotype microarrays revealed that the luxS mutation caused numerous metabolic deficiencies, while AI-3 signaling had little effect on metabolism. This study examines how AI-3 production is affected by the luxS mutation and explores the roles of the LuxS/AI-2 system in metabolism and QS.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

AI-3 Synthesis Is Not Dependent onluxSinEscherichia coli

2006

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“…With the concept of molecular mimicry in hand and the goal of identifying novel antagonists of AI-2 signaling, Wang and colleagues published a series of papers in which they screened a large number of compounds that they believed would have the potential to complex with the V. harveyi receptor LuxP (131,204,205). They chose to focus on compounds with molecular structures significantly different from those of the previously examined nonaromatic cyclic polyols which generally exhibited agonist activity (206)(207)(208). The first two screens involved diol-containing compounds, which have the ability to complex with boric acid, and native boronic acid compounds (131,205), all chosen due to their similarities to the 2,3-borate diester form of AI-2 recognized by LuxP (Fig.…”

Section: Inhibition Of Signal Detection Synthetic Signal Analogues Anmentioning

confidence: 99%

Exploiting Quorum Sensing To Confuse Bacterial Pathogens

LaSarre

Federle

2013

Microbiol Mol Biol Rev

676

556

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SUMMARY Cell-cell communication, or quorum sensing, is a widespread phenomenon in bacteria that is used to coordinate gene expression among local populations. Its use by bacterial pathogens to regulate genes that promote invasion, defense, and spread has been particularly well documented. With the ongoing emergence of antibiotic-resistant pathogens, there is a current need for development of alternative therapeutic strategies. An antivirulence approach by which quorum sensing is impeded has caught on as a viable means to manipulate bacterial processes, especially pathogenic traits that are harmful to human and animal health and agricultural productivity. The identification and development of chemical compounds and enzymes that facilitate quorum-sensing inhibition (QSI) by targeting signaling molecules, signal biogenesis, or signal detection are reviewed here. Overall, the evidence suggests that QSI therapy may be efficacious against some, but not necessarily all, bacterial pathogens, and several failures and ongoing concerns that may steer future studies in productive directions are discussed. Nevertheless, various QSI successes have rightfully perpetuated excitement surrounding new potential therapies, and this review highlights promising QSI leads in disrupting pathogenesis in both plants and animals.

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“…The few known ex-amples of interference with AI-2 often represent more indirect mechanisms, such as inhibition of AI-2 synthesis or phosphorylation processes involved in interspecies signal processes (9,14,45,46). However, several synthetic AI-2 analogues have been shown to compete with natural AI-2 for binding to the corresponding receptor (47)(48)(49)(50). Natural AI-2 signal degradation has been exclusively shown for E. coli LsrG, which catalyzes the cleavage of phosphorylated AI-2, producing 2-phosphoglycolic acid and consequently terminating induction of the lsr operon (49,51).…”

Section: Q Uorum Sensing (Qs) Is the Cell-cell Communication Betweenmentioning

confidence: 99%

Novel Reporter for Identification of Interference with Acyl Homoserine Lactone and Autoinducer-2 Quorum Sensing

Weiland‐Bräuer

Pinnow

Schmitz

2015

Appl Environ Microbiol

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Two reporter strains were established to identify novel biomolecules interfering with bacterial communication (quorum sensing [QS]). The basic design of these Escherichia coli-based systems comprises a gene encoding a lethal protein fused to promoters induced in the presence of QS signal molecules. Consequently, these E. coli strains are unable to grow in the presence of the respective QS signal molecules unless a nontoxic QS-interfering compound is present. The first reporter strain designed to detect autoinducer-2 (AI-2)-interfering activities (AI2-QQ.1) contained the E. coli ccdB lethal gene under the control of the E. coli lsrA promoter. The second reporter strain (AI1-QQ.1) contained the Vibrio fischeri luxI promoter fused to the ccdB gene to detect interference with acyl-homoserine lactones. Bacteria isolated from the surfaces of several marine eukarya were screened for quorum-quenching (QQ) activities using the established reporter systems AI1-QQ.1 and AI2-QQ.1. Out of 34 isolates, two interfered with acylated homoserine lactone (AHL) signaling, five interfered with AI-2 QS signaling, and 10 were demonstrated to interfere with both signal molecules. Open reading frames (ORFs) conferring QQ activity were identified for three selected isolates (Photobacterium sp., Pseudoalteromonas sp., and Vibrio parahaemolyticus). Evaluation of the respective heterologously expressed and purified QQ proteins confirmed their ability to interfere with the AHL and AI-2 signaling processes. Q uorum sensing (QS) is the cell-cell communication betweenbacteria that allows the perception of population density by small signaling molecules-so-called autoinducers-and modifies gene expression in response to the population density. It controls a wide spectrum of processes and phenotypic behaviors, including stress resistance, production of toxins and secondary metabolites, pathogenicity, swarming, and biofilm formation (for a review, see references 1 and 2). In addition to playing important roles in intraspecies and interspecies communication, QS is also involved in host-microbe interactions (3-5). Intraspecific communication of Gram-negative bacteria is based on the production and perception of acylated homoserine lactones (AHLs) synthesized by LuxI homologs. Increasing intracellular concentrations of diffusible AHLs with higher cell densities are perceived by binding of the AHLs to the cognate receptor (e.g., LuxR in Vibrio fischeri), resulting in activation or inhibition of target gene transcription (6, 7). Interspecific communication between different species within one habitat has been demonstrated to depend on the synthesis and detection of the universal autoinducer-2 (AI-2), which can be inhibited by furanones (8, 9). The perception of these signal molecules is achieved either by a two-component regulatory system (e.g., in Vibrio harveyi, where the induced phosphorylation cascade finally results in the induction of specific target genes) (10), or by transportation of the signal molecule into the cell (e.g., in Escherichia coli,...

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Quorum sensing in Vibrio harveyi: probing the specificity of the LuxP binding site

Cited by 45 publications

References 19 publications

AI-3 Synthesis Is Not Dependent onluxSinEscherichia coli

AI-3 Synthesis Is Not Dependent onluxSinEscherichia coli

Exploiting Quorum Sensing To Confuse Bacterial Pathogens

Novel Reporter for Identification of Interference with Acyl Homoserine Lactone and Autoinducer-2 Quorum Sensing

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