Quorum Sensing Controls Biofilm Formation in
            <i>Vibrio cholerae</i>
            through Modulation of Cyclic Di-GMP Levels and Repression of
            <i>vpsT</i>

Waters, Christopher M.; Lu, Wenyun; Rabinowitz, Joshua D.; Bassler, Bonnie L.

doi:10.1128/jb.01756-07

Cited by 373 publications

(447 citation statements)

References 62 publications

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“…To determine which DGCs are enzymatically active in the conditions examined here, each of these expression plasmids was conjugated into the wild type (WT) strain of V. cholerae, and biofilm formation was assessed using a minimum biofilm-eliminating concentration (MBEC) biofilm assay. WT V. cholerae grows to the high-cell-density quorum-sensing state, which represses biofilm formation (20,21). Indeed, the WT strain containing an empty vector control produced minimal biofilms (Fig.…”

Section: Resultsmentioning

confidence: 99%

Quantification of high-specificity cyclic diguanylate signaling

Massie¹,

Reynolds²,

Koestler³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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145

143

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Cyclic di-GMP (c-di-GMP) is a second messenger molecule that regulates the transition between sessile and motile lifestyles in bacteria. Bacteria often encode multiple diguanylate cyclase (DGC) and phosphodiesterase (PDE) enzymes that produce and degrade c-di-GMP, respectively. Because of multiple inputs into the c-di-GMP-signaling network, it is unclear whether this system functions via high or low specificity. High-specificity signaling is characterized by individual DGCs or PDEs that are specifically associated with downstream c-di-GMP-mediated responses. In contrast, low-specificity signaling is characterized by DGCs or PDEs that modulate a general signal pool, which, in turn, controls a global c-di-GMPmediated response. To determine whether c-di-GMP functions via high or low specificity in Vibrio cholerae, we correlated the in vivo c-di-GMP concentration generated by seven DGCs, each expressed at eight different levels, to the c-di-GMP-mediated induction of biofilm formation and transcription. There was no correlation between total intracellular c-di-GMP levels and biofilm formation or gene expression when considering all states. However, individual DGCs showed a significant correlation between c-di-GMP production and c-di-GMP-mediated responses. Moreover, the rate of phenotypic change versus c-di-GMP concentration was significantly different between DGCs, suggesting that bacteria can optimize phenotypic output to c-di-GMP levels via expression or activation of specific DGCs. Our results conclusively demonstrate that c-di-GMP does not function via a simple, low-specificity signaling pathway in V. cholerae.signaling specificity | systems biology

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Section: Resultsmentioning

confidence: 99%

Quantification of high-specificity cyclic diguanylate signaling

Massie¹,

Reynolds²,

Koestler³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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145

143

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“…As a class of bacterial intracellular lipid signals, AHLs are used by gram-negative bacteria to monitor the bacterial population density or to coordinate bacterial social behaviors (Waters and Bassler, 2005;Waters et al, 2008). Recently, more evidence demonstrate that AHLs are able to modulate plant growth and development (Mathesius et al, 2003;Ortíz-Castro et al, 2008;von Rad et al, 2008;Méndez-Bravo et al, 2010;MorquechoContreras et al, 2010).…”

Section: -O-c10-hl Promotes Polar Auxin Transportmentioning

confidence: 99%

“…The basic structure of the AHL family consists of a conserved homoserine-lactone ring and a four-to 18-carbon chain with an amide (N)-linked acyl side group. The acyl side group can be substituted with an oxo or hydroxyl group at position C3 (Waters and Bassler, 2005;Waters et al, 2008). In Arabidopsis (Arabidopsis thaliana), the branched carbonyl chain length influences the biological effects of AHLs, and N-decanoyl-homoserine-lactone (C10-HL) is the most active one for primary root growth and lateral root development (Ortíz-Castro et al, 2008).…”

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confidence: 99%

N-3-Oxo-Decanoyl-l-Homoserine-Lactone Activates Auxin-Induced Adventitious Root Formation via Hydrogen Peroxide- and Nitric Oxide-Dependent Cyclic GMP Signaling in Mung Bean

et al. 2011

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N-Acyl-homoserine-lactones (AHLs) are bacterial quorum-sensing signaling molecules that regulate population density. Recent evidence demonstrates their roles in plant defense responses and root development. Hydrogen peroxide (H 2 O 2 ), nitric oxide (NO), and cyclic GMP (cGMP) are essential messengers that participate in various plant physiological processes, but how these messengers modulate the plant response to N-acyl-homoserine-lactone signals remains poorly understood. Here, we show that the N-3-oxo-decanoyl-homoserine-lactone (3-O-C10-HL), in contrast to its analog with an unsubstituted branch chain at the C3 position, efficiently stimulated the formation of adventitious roots and the expression of auxin-response genes in explants of mung bean (Vigna radiata) seedlings. This response was mimicked by the exogenous application of auxin, H 2 O 2 , NO, or cGMP homologs but suppressed by treatment with scavengers or inhibitors of H 2 O 2 , NO, or cGMP metabolism. The 3-O-C10-HL treatment enhanced auxin basipetal transport; this effect could be reversed by treatment with H 2 O 2 or NO scavengers but not by inhibitors of cGMP synthesis. Inhibiting 3-O-C10-HL-induced H 2 O 2 or NO accumulation impaired auxin-or 3-O-C10-HL-induced cGMP synthesis; however, blocking cGMP synthesis did not affect auxin-or 3-O-C10-HLinduced H 2 O 2 or NO generation. Additionally, cGMP partially rescued the inhibitory effect of H 2 O 2 or NO scavengers on 3-O-C10-HL-induced adventitious root development and auxin-response gene expression. These results suggest that 3-O-C10-HL, unlike its analog with an unmodified branch chain at the C3 position, can accelerate auxin-dependent adventitious root formation, possibly via H 2 O 2 -and NO-dependent cGMP signaling in mung bean seedlings.

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“…Key to this regulation is cell density-dependent cell-to-cell signalling, which is termed quorum sensing (QS) (Rumbaugh et al, 2000). As in many other bacteria, QS controls secretion of virulence factors (Mittal et al, 2006), biofilm formation (Waters et al, 2008) and the exchange of DNA (Fuqua & Winans, 1996) in P. aeruginosa. The biofilm mode of growth is recognized as an important bacterial trait that is relevant to infections (Costerton et al, 1994).…”

mentioning

confidence: 99%

Screening for novel quorum-sensing inhibitors to interfere with the formation of Pseudomonas aeruginosa biofilm

Ding

Yin

et al. 2011

Journal of Medical Microbiology

126

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The objective of this study was to screen for novel quorum-sensing inhibitors (QSIs) from traditional Chinese medicines (TCMs) that inhibit bacterial biofilm formation. Six of 46 active components found in TCMs were identified as putative QSIs based on molecular docking studies. Of these, three compounds inhibited biofilm formation by Pseudomonas aeruginosa and Stenotrophomonas maltophilia at a concentration of 200 mM. A fourth compound (emodin) significantly inhibited biofilm formation at 20 mM and induced proteolysis of the quorum-sensing signal receptor TraR in Escherichia coli at a concentration of 3-30 mM. Emodin also increased the activity of ampicillin against P. aeruginosa. Therefore, emodin might be suitable for development into an antivirulence and antibacterial agent. INTRODUCTIONPseudomonas aeruginosa, an opportunistic human pathogen, may cause acute infections in hospitalized patients, can be isolated from the environment, particularly from soil and water, and it regularly contaminates medical devices (Stover et al., 2000). It is also the predominant cause of chronic lung infection in cystic fibrosis patients (Frederiksen et al., 1997) and has recently been recognized as one of the main causes of chronic wound infections (Gjødsbøl et al., 2006). P. aeruginosa can infect patients by producing a wide range of virulence factors, the expression levels of which are tightly regulated. Key to this regulation is cell density-dependent cell-to-cell signalling, which is termed quorum sensing (QS) (Rumbaugh et al., 2000). As in many other bacteria, QS controls secretion of virulence factors (Mittal et al., 2006), biofilm formation (Waters et al., 2008) and the exchange of DNA (Fuqua & Winans, 1996) in P. aeruginosa. The biofilm mode of growth is recognized as an important bacterial trait that is relevant to infections (Costerton et al., 1994). Many infections involve the formation of bacterial biofilms, which are bacterial communities that settle and proliferate on surfaces and are covered by exopolymers (Lewis, 2007). Once established, biofilms are difficult to eradicate and become a source of secondary infection (Jones et al., 2009). Moreover, bacteria embedded in biofilms are more tolerant than planktonic cells of antibiotics (Donlan & Costerton, 2002;Drenkard, 2003). The dose of antibiotics needed in this situation will often exceed the highest deliverable dose, which makes efficient treatment impossible.QS, as a regulatory mechanism, enables bacteria to make collective decisions with respect to the expression of a specific set of genes that involve the production, release and subsequent detection of chemical signalling molecules, such as N-acylhomoserine lactones (AHLs) that are commonly used by Gram-negative bacteria. When the concentration of AHLs reaches a certain threshold level, binding to a receptor molecule (for example, LuxR) is promoted and the activated LuxR-AHL complex forms dimers or polymers, which, in turn, act as transcriptional regulators of target genes in the QS regulon (Parsek & Greenbe...

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Quorum Sensing Controls Biofilm Formation in Vibrio cholerae through Modulation of Cyclic Di-GMP Levels and Repression of vpsT

Cited by 373 publications

References 62 publications

Quantification of high-specificity cyclic diguanylate signaling

Quantification of high-specificity cyclic diguanylate signaling

N-3-Oxo-Decanoyl-l-Homoserine-Lactone Activates Auxin-Induced Adventitious Root Formation via Hydrogen Peroxide- and Nitric Oxide-Dependent Cyclic GMP Signaling in Mung Bean

Screening for novel quorum-sensing inhibitors to interfere with the formation of Pseudomonas aeruginosa biofilm

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