Dataset Information

Biofilm formation in marine bacteria and biocidal sensitivity: interplay between a potent antibiofilm compound (AS162) and quorum-sensing autoinducers.

ABSTRACT: The capacity of two homoserine lactones to stimulate the marine bacteria Pseudoalteromonas ulvae (TC14 strain) for its capacity to form a biofilm when exposed to a potent antibiofilm compound AS162 is reported. Effective concentrations (EC₅₀) of AS162 at 24 h, 48 h, and 72 h were, respectively, of 4.3, 4.4, and 6.0 µM. When tested in combination with HSLs, results showed that quorum-sensing signal molecules 3-oxo-C6 and 3-oxo-C8 homoserine lactones do not act directly on the biofilm formation, but are able to interfere positively with AS162 to promote biofilm growth with EC₅₀ ranging from 30 to 50 µM. The same results were obtained with two other marine bacterial strains: Pseudoalteromonas lipolytica TC8 and Paracoccus sp. 4M6. These findings suggest that HSLs can significantly affect the biocidal sensitivity of marine bacteria to antifouling agents.

SUBMITTER: Gozoua E

PROVIDER: S-EPMC6701715 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Biofilm formation in marine bacteria and biocidal sensitivity: interplay between a potent antibiofilm compound (AS162) and quorum-sensing autoinducers.

Gozoua Emmanuel E Koffi-Nevry Rose R Blache Yves Y

3 Biotech 20190819 9

The capacity of two homoserine lactones to stimulate the marine bacteria <i>Pseudoalteromonas ulvae</i> (TC14 strain) for its capacity to form a biofilm when exposed to a potent antibiofilm compound AS162 is reported. Effective concentrations (EC<sub>50</sub>) of AS162 at 24 h, 48 h, and 72 h were, respectively, of 4.3, 4.4, and 6.0 µM. When tested in combination with HSLs, results showed that quorum-sensing signal molecules 3-oxo-C6 and 3-oxo-C8 homoserine lactones do not act directly on the bi ...[more]

PMID: 31467830

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Project description:Vibrio cholerae possesses multiple quorum-sensing (QS) systems that control virulence and biofilm formation among other traits. At low cell densities, when QS 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 QS autoinducers that function in parallel. One autoinducer, called cholerae autoinducer-1 (CAI-1), is used to measure Vibrio abundance, and the other autoinducer, called autoinducer-2 (AI-2), is widely produced by different bacterial species and 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 QS 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 QS to distinguish kin from nonkin 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 QS 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 QS 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 QS mode, but it is, in fact, the broadly made autoinducer AI-2 that sets the pace of the V. cholerae QS program. This first report of unique roles for the different V. cholerae autoinducers suggests that detection of kin fosters a distinct outcome from detection of nonkin.

Project description:Quorum sensing (QS) is a process of cell-to-cell communication that bacteria use to orchestrate collective behaviors. QS relies on the cell-density-dependent production, accumulation, and receptor-mediated detection of extracellular signaling molecules called autoinducers (AIs). Gram-negative bacteria commonly use N-acyl homoserine lactones (AHLs) as their AIs, and they are detected by LuxR-type receptors. Often, LuxR-type receptors are insoluble when not bound to a cognate AI. In this report, we show that LuxR-type receptors are encoded on phage genomes, and in the cases we tested, the phage LuxR-type receptors bind to and are solubilized specifically by the AHL AI produced by the host bacterium. We do not yet know the viral activities that are controlled by these phage QS receptors; however, our observations, coupled with recent reports, suggest that their occurrence is more widespread than previously appreciated. Using receptor-mediated detection of QS AIs could enable phages to garner information concerning the population density status of their bacterial hosts. We speculate that such information can be exploited by phages to optimize the timing of execution of particular steps in viral infection.IMPORTANCE Bacteria communicate with chemical signal molecules to regulate group behaviors in a process called quorum sensing (QS). In this report, we find that genes encoding receptors for Gram-negative bacterial QS communication molecules are present on genomes of viruses that infect these bacteria. These viruses are called phages. We show that two phage-encoded receptors, like their bacterial counterparts, bind to the communication molecule produced by the host bacterium, suggesting that phages can "listen in" on their bacterial hosts. Interfering with bacterial QS and using phages to kill pathogenic bacteria represent attractive possibilities for development of new antimicrobials to combat pathogens that are resistant to traditional antibiotics. Our findings of interactions between phages and QS bacteria need consideration as new antimicrobial therapies are developed.

Dataset Information

Biofilm formation in marine bacteria and biocidal sensitivity: interplay between a potent antibiofilm compound (AS162) and quorum-sensing autoinducers.

Publications

Biofilm formation in marine bacteria and biocidal sensitivity: interplay between a potent antibiofilm compound (AS162) and quorum-sensing autoinducers.

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