scholarly journals Quorum Sensing System of Ruegeria mobilis Rm01 Controls Lipase and Biofilm Formation

2019 ◽  
Vol 9 ◽  
Author(s):  
Ying Su ◽  
Kaihao Tang ◽  
Jiwen Liu ◽  
Yan Wang ◽  
Yanfen Zheng ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Biofilm Formation ◽  
Sensing System ◽  
Quorum Sensing System

The intra-genus and inter-species quorum-sensing autoinducers exert distinct control over Vibrio cholerae biofilm formation and dispersal

2019 ◽  
Author(s):  
Andrew A. Bridges ◽  
Bonnie L. Bassler
Keyword(s):  
Quorum Sensing ◽  
Vibrio Cholerae ◽  
Cell Density ◽  
Biofilm Formation ◽  
Specific Information ◽  
High Cell ◽  
Coincidence Detector ◽  
Sensing System ◽  
Quorum Sensing System ◽  
Cell Densities

AbstractVibrio cholerae possesses multiple quorum-sensing systems that control virulence and biofilm formation among other traits. At low cell densities, when quorum-sensing autoinducers are absent, V. cholerae forms biofilms. At high cell densities, when autoinducers have accumulated, biofilm formation is repressed and dispersal occurs. Here, we focus on the roles of two well-characterized quorum-sensing autoinducers that function in parallel. One autoinducer, called CAI-1, is used to measure vibrio abundance, and the other autoinducer, called AI-2, is a broadly-made universal autoinducer that is presumed to enable V. cholerae to assess the total bacterial cell density of the vicinal community. The two V. cholerae autoinducers funnel information into a shared signal relay pathway. This feature of the quorum-sensing system architecture has made it difficult to understand how specific information can be extracted from each autoinducer, how the autoinducers might drive distinct output behaviors, and in turn, how the bacteria use quorum sensing to distinguish self from other in bacterial communities. We develop a live-cell biofilm formation and dispersal assay that allows examination of the individual and combined roles of the two autoinducers in controlling V. cholerae behavior. We show that the quorum-sensing system works as a coincidence detector in which both autoinducers must be present simultaneously for repression of biofilm formation to occur. Within that context, the CAI-1 quorum-sensing pathway is activated when only a few V. cholerae cells are present, whereas the AI-2 pathway is activated only at much higher cell density. The consequence of this asymmetry is that exogenous sources of AI-2, but not CAI-1, contribute to satisfying the coincidence detector to repress biofilm formation and promote dispersal. We propose that V. cholerae uses CAI-1 to verify that some of its kin are present before committing to the high-cell-density quorum-sensing mode, but it is, in fact, the universal autoinducer AI-2, that sets the pace of the V. cholerae quorum-sensing program. This first report of unique roles for the different V. cholerae autoinducers suggests that detection of self fosters a distinct outcome from detection of other.

scholarly journals The LuxS-Dependent Quorum-Sensing System Regulates Early Biofilm Formation by Streptococcus pneumoniae Strain D39

2011 ◽  
Vol 79 (10) ◽  
pp. 4050-4060 ◽  
Author(s):  
Jorge E. Vidal ◽  
Herbert P. Ludewick ◽  
Rebekah M. Kunkel ◽  
Dorothea Zähner ◽  
Keith P. Klugman
Keyword(s):  
Streptococcus Pneumoniae ◽  
Quorum Sensing ◽  
Biofilm Formation ◽  
Single Copy ◽  
Middle Ear Mucosa ◽  
Transcript Levels ◽  
Content Type ◽  
Sensing System ◽  
Quorum Sensing System

ABSTRACTStreptococcus pneumoniaeis the leading cause of death in children worldwide and forms highly organized biofilms in the nasopharynx, lungs, and middle ear mucosa. TheluxS-controlled quorum-sensing (QS) system has recently been implicated in virulence and persistence in the nasopharynx, but its role in biofilms has not been studied. Here we show that this QS system plays a major role in the control ofS. pneumoniaebiofilm formation. Our results demonstrate that theluxSgene is contained by invasive isolates and normal-flora strains in a region that contains genes involved in division and cell wall biosynthesis. TheluxSgene was maximally transcribed, as a monocistronic message, in the early mid-log phase of growth, and this coincides with the appearance of early biofilms. Demonstrating the role of the LuxS system in regulatingS. pneumoniaebiofilms, at 24 h postinoculation, two different D39ΔluxSmutants produced ∼80% less biofilm biomass than wild-type (WT) strain D39 did. Complementation of these strains withluxS, either in a plasmid or integrated as a single copy in the genome, restored their biofilm level to that of the WT. Moreover, a soluble factor secreted by WT strain D39 or purified AI-2 restored the biofilm phenotype of D39ΔluxS. Our results also demonstrate that during the early mid-log phase of growth, LuxS regulates the transcript levels oflytA, which encodes an autolysin previously implicated in biofilms, and also the transcript levels ofply, which encodes the pneumococcal pneumolysin. In conclusion, theluxS-controlled QS system is a key regulator of early biofilm formation byS. pneumoniaestrain D39.

scholarly journals The Plant Pathogen Pantoea ananatis Produces N-Acylhomoserine Lactone and Causes Center Rot Disease of Onion by Quorum Sensing

2007 ◽  
Vol 189 (22) ◽  
pp. 8333-8338 ◽  
Author(s):  
Tomohiro Morohoshi ◽  
Yuta Nakamura ◽  
Go Yamazaki ◽  
Akio Ishida ◽  
Norihiro Kato ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Biofilm Formation ◽  
Receptor Gene ◽  
Homoserine Lactone ◽  
Pantoea Ananatis ◽  
Signal Molecule ◽  
Acylhomoserine Lactone ◽  
Sensing System ◽  
Quorum Sensing System ◽  
Rot Disease

ABSTRACT A number of gram-negative bacteria have a quorum-sensing system and produce N-acyl-l-homoserine lactone (AHL) that they use them as a quorum-sensing signal molecule. Pantoea ananatis is reported as a common colonist of wheat heads at ripening and causes center rot of onion. In this study, we demonstrated that P. ananatis SK-1 produced two AHLs, N-hexanoyl-l-homoserine lactone (C6-HSL) and N-(3-oxohexanoyl)-l-homoserine lactone (3-oxo-C6-HSL). We cloned the AHL-synthase gene (eanI) and AHL-receptor gene (eanR) and revealed that the deduced amino acid sequence of EanI/EanR showed high identity to those of EsaI/EsaR from P. stewartii. EanR repressed the ean box sequence and the addition of AHLs resulted in derepression of ean box. Inactivation of the chromosomal eanI gene in SK-1 caused disruption of exopolysaccharide (EPS) biosynthesis, biofilm formation, and infection of onion leaves, which were recovered by adding exogenous 3-oxo-C6-HSL. These results demonstrated that the quorum-sensing system involved the biosynthesis of EPS, biofilm formation, and infection of onion leaves in P. ananatis SK-1.

scholarly journals N-Octanoylhomoserine lactone signalling mediated by the BpsI–BpsR quorum sensing system plays a major role in biofilm formation of Burkholderia pseudomallei

Microbiology ◽  
2011 ◽  
Vol 157 (4) ◽  
pp. 1176-1186 ◽  
Author(s):  
Akshamal Mihiranga Gamage ◽  
Guanghou Shui ◽  
Markus R. Wenk ◽  
Kim Lee Chua
Keyword(s):  
Quorum Sensing ◽  
Biofilm Formation ◽  
Burkholderia Pseudomallei ◽  
Homoserine Lactone ◽  
Tandem Ms ◽  
Wild Type ◽  
Acylhomoserine Lactone ◽  
Sensing System ◽  
Sensing Systems ◽  
Quorum Sensing System

The genome of Burkholderia pseudomallei encodes three acylhomoserine lactone (AHL) quorum sensing systems, each comprising an AHL synthase and a signal receptor/regulator. The BpsI–BpsR system produces N-octanoylhomoserine lactone (C8HL) and is positively auto-regulated by its AHL product. The products of the remaining two systems have not been identified. In this study, tandem MS was used to identify and quantify the AHL species produced by three clinical B. pseudomallei isolates – KHW, K96243 and H11 – three isogenic KHW mutants that each contain a null mutation in an AHL synthase gene, and recombinant Escherichia coli heterologously expressing each of the three B. pseudomallei AHL synthase genes. BpsI synthesized predominantly C8HL, which accounted for more than 95 % of the extracellular AHLs produced in stationary-phase KHW cultures. The major products of BpsI2 and BpsI3 were N-(3-hydroxy-octanoyl)homoserine lactone (OHC8HL) and N-(3-hydroxy-decanoyl)homoserine lactone, respectively, and their corresponding transcriptional regulators, BpsR2 and BpsR3, were capable of driving reporter gene expression in the presence of these cognate lactones. Formation of biofilm by B. pseudomallei KHW was severely impaired in mutants lacking either BpsI or BpsR but could be restored to near wild-type levels by exogenous C8HL. BpsI2 was not required, and BpsI3 was partially required for biofilm formation. Unlike the bpsI mutant, biofilm formation in the bpsI3 mutant could not be restored to wild-type levels in the presence of OHC8HL, the product of BpsI3. C8HL and OHC8HL had opposite effects on biofilm formation; exogenous C8HL enhanced biofilm formation in both the bpsI3 mutant and wild-type KHW while exogenous OHC8HL suppressed the formation of biofilm in the same strains. We propose that exogenous OHC8HL antagonizes biofilm formation in B. pseudomallei, possibly by competing with endogenous C8HL for binding to BpsR.

scholarly journals Role of the luxS Quorum-Sensing System in Biofilm Formation and Virulence of Staphylococcus epidermidis

2006 ◽  
Vol 74 (1) ◽  
pp. 488-496 ◽  
Author(s):  
Lin Xu ◽  
Hualin Li ◽  
Cuong Vuong ◽  
Viveka Vadyvaloo ◽  
Jianping Wang ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Mutant Strain ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Bacterial Pathogens ◽  
Sensing System ◽  
Autoinducer 2 ◽  
Enhanced Production ◽  
Quorum Sensing System ◽  
Biofilm Development

ABSTRACT Nosocomial infections caused by Staphylococcus epidermidis are characterized by biofilm formation on implanted medical devices. Quorum-sensing regulation plays a major role in the biofilm development of many bacterial pathogens. Here, we describe luxS, a quorum-sensing system in staphylococci that has a significant impact on biofilm development and virulence. We constructed an isogenic ΔluxS mutant strain of a biofilm-forming clinical isolate of S. epidermidis and demonstrated that luxS signaling is functional in S. epidermidis. The mutant strain showed increased biofilm formation in vitro and enhanced virulence in a rat model of biofilm-associated infection. Genetic complementation and addition of autoinducer 2-containing culture filtrate restored the wild-type phenotype, demonstrating that luxS repressed biofilm formation through a cell-cell signaling mechanism based on autoinducer 2 secretion. Enhanced production of the biofilm exopolysaccharide polysaccharide intercellular adhesin in the mutant strain is presumably the major cause of the observed phenotype. The agr quorum-sensing system has previously been shown to impact biofilm development and biofilm-associated infection in a way similar to that of luxS, although by regulation of different factors. Our study indicates a general scheme of quorum-sensing regulation of biofilm development in staphylococci, which contrasts with that observed in many other bacterial pathogens.

scholarly journals Pseudomonas aeruginosa synthesizes the autoinducers of its oxylipin-dependent quorum sensing system extracellularly

2021 ◽  
Author(s):  
Eriel Martínez ◽  
Carlos J. Orihuela ◽  
Javier Campos-Gomez
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Outer Membrane ◽  
Biofilm Formation ◽  
Octadecenoic Acid ◽  
Secretion System ◽  
Genetic Screen ◽  
Dependent Manner ◽  
Sensing System ◽  
Quorum Sensing System

ABSTRACTThe oxylipin-dependent quorum sensing system (ODS) of Pseudomonas aeruginosa relies on the production and sensing of two oxylipin autoinducers, 10S-hydroxy-(8E)-octadecenoic acid (10-HOME) and 7S,10S dihydroxy-(8E)-octadecenoic acid (7,10-DiHOME). Here, and contrary to the prevailing notion that bacterial autoinducers are synthesized intracellularly, we show that 10-HOME and 7,10-DiHOME biosynthesis occurs extracellularly, and this requires the secretion of the oxylipin synthases. We implemented a genetic screen of P. aeruginosa strain PAO1, which identified fourteen genes required for the synthesis of oxylipins. Among the identified genes, four encoded components of the ODS system and the other ten were part of the Xcp type II secretion system (T2SS). We created a deletion mutant of xcpQ, which encodes the outer membrane component of Xcp, and found it recapitulated the impaired functionality of the transposon mutants. Upon further examination, the lack of ODS function was demonstrated to be caused by the blocking of the DS enzymes secretion. Notably, the xcpQ mutant activated the ODS system when exposed to 10-HOME and 7,10-DiHOME, indicating that the sensing component of this quorum sensing system remains fully functional. In contrast with the detrimental effect previously described for T2SS in biofilm formation, here we observed that T2SS was required for robust in vitro and in vivo biofilm formation in an ODS dependent manner. To the best of our knowledge, this study is the first to find QS autoinducers that are synthetized in the extracellular space and provides new evidence for the role of the T2SS for biofilm formation in P. aeruginosa.IMPORTANCEWe previously showed that the ODS quorum sensing system of P. aeruginosa produces and responds to oxylipins derived from host oleic acid by enhancing biofilm formation and virulence. Herein, we developed a genetic screen strategy to explore the molecular basis for oxylipins synthesis and detection. Unexpectedly, we found that the ODS autoinducer synthases cross the outer membrane using the Xcp Type 2 secretion system of P. aeruginosa and thus, the biosynthesis of oxylipins occur extracellularly. Biofilm formation, which was thought to be impaired as result of Xcp activity, was found to be enhanced as result of ODS activation. This is a unique QS system strategy and reveals a new way by which P. aeruginosa interacts with the host environment.

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