scholarly journals Vibrio cholerae OmpR Contributes to Virulence Repression and Fitness at Alkaline pH

2020 ◽  
Vol 88 (6) ◽  
Author(s):  
D. E. Kunkle ◽  
X. R. Bina ◽  
J. E. Bina
Keyword(s):  
Vibrio Cholerae ◽  
Marine Ecosystem ◽  
Acid Tolerance ◽  
Alkaline Ph ◽  
Adaptive Responses ◽  
Gram Negative ◽  
Content Type ◽  
Regulatory Systems ◽  
Contaminated Food ◽  
Alkaline Conditions

ABSTRACT Vibrio cholerae is a Gram-negative human pathogen and the causative agent of the life-threatening disease cholera. V. cholerae is a natural inhabitant of marine environments and enters humans through the consumption of contaminated food or water. The ability to transition between aquatic ecosystems and the human host is paramount to the pathogenic success of V. cholerae. The transition between these two disparate environments requires the expression of adaptive responses, and such responses are most often regulated by two-component regulatory systems such as the EnvZ/OmpR system, which responds to osmolarity and acidic pH in many Gram-negative bacteria. Previous work in our laboratory indicated that V. cholerae OmpR functioned as a virulence regulator through repression of the LysR-family transcriptional regulator aphB; however, the role of OmpR in V. cholerae biology outside virulence regulation remained unknown. In this work, we sought to further investigate the function of OmpR in V. cholerae biology by defining the OmpR regulon through RNA sequencing. This led to the discovery that V. cholerae ompR was induced at alkaline pH to repress genes involved in acid tolerance and virulence factor production. In addition, OmpR was required for V. cholerae fitness during growth under alkaline conditions. These findings indicate that V. cholerae OmpR has evolved the ability to respond to novel signals during pathogenesis, which may play a role in the regulation of adaptive responses to aid in the transition between the human gastrointestinal tract and the marine ecosystem.

scholarly journals The Outer Surface Lipoprotein VolA Mediates Utilization of Exogenous Lipids by Vibrio cholerae

mBio ◽  
2013 ◽  
Vol 4 (3) ◽  
Author(s):  
Aaron C. Pride ◽  
Carmen M. Herrera ◽  
Ziqiang Guan ◽  
David K. Giles ◽  
M. Stephen Trent
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Carbon Source ◽  
Outer Membrane ◽  
Vibrio Cholerae ◽  
Homeoviscous Adaptation ◽  
Gram Negative ◽  
Content Type ◽  
Enzymatic Function ◽  
Gram Negative Organisms

ABSTRACTPrevious work from our laboratory showed that the Gram-negative aquatic pathogenVibrio choleraecan take up a much wider repertoire of fatty acids than other Gram-negative organisms. The current work elaborated on the ability ofV. choleraeto exploit an even more diverse pool of lipid nutrients from its environment. We have demonstrated that the bacterium can use lysophosphatidylcholine as a metabolite for growth. Using a combination of thin-layer chromatography and mass spectrometry, we also showed that lysophosphatidylcholine-derived fatty acid moieties can be used for remodeling theV. choleraemembrane architecture. Furthermore, we have identified a lysophospholipase, VolA (Vibrioouter membrane lysophospholipase A), required for these activities. The enzyme is well conserved inVibriospecies, is coexpressed with the outer membrane fatty acid transporter FadL, is one of very few surface-exposed lipoprotein enzymes to be identified in Gram-negative bacteria and the first instance of a surface lipoprotein phospholipase. We propose a model whereby the bacterium efficiently couples the liberation of fatty acid from lysophosphatidylcholine to its subsequent metabolic uptake. An expanded ability to scavenge diverse environmental lipids at the bacterial surface increases overall bacterial fitness and promotes homeoviscous adaptation through membrane remodeling.IMPORTANCEOur understanding of how bacteria utilize environmental lipid sources has been limited to lipids such as fatty acids and cholesterol. This narrow scope may be attributed to both the intricate nature of lipid uptake mechanisms and the diversity of lipid substrates encountered within an ecological niche. By examining the ability of the pathogenVibrio choleraeto utilize exogenous lipids, we uncovered a surface-exposed lipoprotein (VolA) that is required for processing the prevalent host lipid lysophosphatidylcholine. VolA functions as a lipase liberating a fatty acid from exogenous lysophospholipids. The freed fatty acid is then transported into the cell, serving as a carbon source, or shunted into phospholipid synthesis for membrane assembly. A limited number of surface-exposed lipoproteins have been found in Gram-negative organisms, and few have enzymatic function. This work highlights the ability of bacteria to exploit exogenous lipids for both maintenance of the membrane and carbon source acquisition.

scholarly journals TheBeauveria bassianaGas3 β-Glucanosyltransferase Contributes to Fungal Adaptation to Extreme Alkaline Conditions

2018 ◽  
Vol 84 (15) ◽  
Author(s):  
Zhibing Luo ◽  
Tongbing Zhang ◽  
Pengfei Liu ◽  
Yuting Bai ◽  
Qiyan Chen ◽  
...  
Keyword(s):  
Cell Wall ◽  
Pathogenic Fungus ◽  
Growth Conditions ◽  
Alkaline Ph ◽  
Ph Responsive ◽  
Content Type ◽  
Cell Wall Remodeling ◽  
Alkaline Conditions ◽  
Increased Sensitivity ◽  
Ph Dependent

ABSTRACTFungal β-1,3-glucanosyltransferases are cell wall-remodeling enzymes implicated in stress response, cell wall integrity, and virulence, with most fungal genomes containing multiple members. The insect-pathogenic fungusBeauveria bassianadisplays robust growth over a wide pH range (pH 4 to 10). A random insertion mutant library screening for increased sensitivity to alkaline (pH 10) growth conditions resulted in the identification and mapping of a mutant to a β-1,3-glucanosyltransferase gene (Bbgas3).Bbgas3expression was pH dependent and regulated by the PacC transcription factor, which activates genes in response to neutral/alkaline growth conditions. Targeted gene knockout ofBbgas3resulted in reduced growth under alkaline conditions, with only minor effects of increased sensitivity to cell wall stress (Congo red and calcofluor white) and no significant effects on fungal sensitivity to oxidative or osmotic stress. The cell walls of ΔBbgas3aerial conidia were thinner than those of the wild-type and complemented strains in response to alkaline conditions, and β-1,3-glucan antibody and lectin staining revealed alterations in cell surface carbohydrate epitopes. The ΔBbgas3mutant displayed alterations in cell wall chitin and carbohydrate content in response to alkaline pH. Insect bioassays revealed impaired virulence for the ΔBbgas3mutant depending upon the pH of the media on which the conidia were grown and harvested. Unexpectedly, a decreased median lethal time to kill (LT50, i.e., increased virulence) was seen for the mutant using intrahemocoel injection assays using conidia grown at acidic pH (5.6). These data show that BbGas3 acts as a pH-responsive cell wall-remodeling enzyme involved in resistance to extreme pH (>9).IMPORTANCELittle is known about adaptations required for growth at high (>9) pH. Here, we show that a specific fungal membrane-remodeling β-1,3-glucanosyltransferase gene (Bbgas3) regulated by the pH-responsive PacC transcription factor forms a critical aspect of the ability of the insect-pathogenic fungusBeauveria bassianato grow at extreme pH. The loss ofBbgas3resulted in a unique decreased ability to grow at high pH, with little to no effects seen with respect to other stress conditions, i.e., cell wall integrity and osmotic and oxidative stress. However, pH-dependent alternations in cell wall properties and virulence were noted for the ΔBbgas3 mutant. These data provide a mechanistic insight into the importance of the specific cell wall structure required to stabilize the cell at high pH and link it to the PacC/Pal/Rim pH-sensing and regulatory system.

scholarly journals Escherichia coli YqjA, a Member of the Conserved DedA/Tvp38 Membrane Protein Family, Is a Putative Osmosensing Transporter Required for Growth at Alkaline pH

2015 ◽  
Vol 197 (14) ◽  
pp. 2292-2300 ◽  
Author(s):  
Sujeet Kumar ◽  
William T. Doerrler
Keyword(s):  
Escherichia Coli ◽  
Membrane Protein ◽  
Amino Acid Identity ◽  
Protein Family ◽  
Cytoplasmic Ph ◽  
Alkaline Ph ◽  
Ph Homeostasis ◽  
Content Type ◽  
E Coli ◽  
Alkaline Conditions

ABSTRACTThe ability to persist and grow under alkaline conditions is an important characteristic of many bacteria. In order to survive at alkaline pH,Escherichia colimust maintain a stable cytoplasmic pH of about 7.6. Membrane cation/proton antiporters play a major role in alkaline pH homeostasis by catalyzing active inward proton transport. The DedA/Tvp38 family is a highly conserved membrane protein family of unknown function present in most sequenced genomes. YqjA and YghB are members of theE. coliDedA family with 62% amino acid identity and partially redundant functions. We have shown thatE. coliwith ΔyqjAand ΔyghBmutations cannot properly maintain the proton motive force (PMF) and is compromised in PMF-dependent drug efflux and other PMF-dependent functions. Furthermore, the functions of YqjA and YghB are dependent upon membrane-embedded acidic amino acids, a hallmark of several families of proton-dependent transporters. Here, we show that the ΔyqjAmutant (but not ΔyghB) cannot grow under alkaline conditions (ranging from pH 8.5 to 9.5), unlike the parentE. coli. Overexpression ofyqjArestores growth at alkaline pH, but only when more than ∼100 mM sodium or potassium is present in the growth medium. Increasing the osmotic pressure by the addition of sucrose enhances the ability of YqjA to support growth under alkaline conditions in the presence of low salt concentrations, consistent with YqjA functioning as an osmosensor. We suggest that YqjA possesses proton-dependent transport activity that is stimulated by osmolarity and that it plays a significant role in the survival ofE. coliat alkaline pH.IMPORTANCEThe ability to survive under alkaline conditions is important for many species of bacteria.Escherichia colican grow at pH 5.5 to 9.5 while maintaining a constant cytoplasmic pH of about 7.6. Under alkaline conditions, bacteria rely upon proton-dependent transporters to maintain a constant cytoplasmic pH. The DedA/Tvp38 protein family is a highly conserved but poorly characterized family of membrane proteins. Here, we show that the DedA/Tvp38 protein YqjA is critical forE. colito survive at pH 8.5 to 9.5. YqjA requires sodium and potassium for this function. At low cation concentrations, osmolytes, including sucrose, can facilitate rescue ofE. coligrowth by YqjA at high pH. These data are consistent with YqjA functioning as an osmosensing cation-dependent proton transporter.

scholarly journals Antibiotic Korormicin A Kills Bacteria by Producing Reactive Oxygen Species

2019 ◽  
Vol 201 (11) ◽  
Author(s):  
Adam Maynard ◽  
Nicole L. Butler ◽  
Takeshi Ito ◽  
Adilson José da Silva ◽  
Masatoshi Murai ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Pseudomonas Aeruginosa ◽  
Vibrio Cholerae ◽  
Pathogenic Bacteria ◽  
Reactive Oxygen ◽  
Direct Result ◽  
Oxygen Species ◽  
Gram Negative ◽  
Content Type ◽  
Nadh:Quinone Oxidoreductase

ABSTRACT Korormicin is an antibiotic produced by some pseudoalteromonads which selectively kills Gram-negative bacteria that express the Na+-pumping NADH:quinone oxidoreductase (Na+-NQR.) We show that although korormicin is an inhibitor of Na+-NQR, the antibiotic action is not a direct result of inhibiting enzyme activity. Instead, perturbation of electron transfer inside the enzyme promotes a reaction between O2 and one or more redox cofactors in the enzyme (likely the flavin adenine dinucleotide [FAD] and 2Fe-2S center), leading to the production of reactive oxygen species (ROS). All Pseudoalteromonas contain the nqr operon in their genomes, including Pseudoalteromonas strain J010, which produces korormicin. We present activity data indicating that this strain expresses an active Na+-NQR and that this enzyme is not susceptible to korormicin inhibition. On the basis of our DNA sequence data, we show that the Na+-NQR of Pseudoalteromonas J010 carries an amino acid substitution (NqrB-G141A; Vibrio cholerae numbering) that in other Na+-NQRs confers resistance against korormicin. This is likely the reason that a functional Na+-NQR is able to exist in a bacterium that produces a compound that typically inhibits this enzyme and causes cell death. Korormicin is an effective antibiotic against such pathogens as Vibrio cholerae, Aliivibrio fischeri, and Pseudomonas aeruginosa but has no effect on Bacteroides fragilis and Bacteroides thetaiotaomicron, microorganisms that are important members of the human intestinal microflora. IMPORTANCE As multidrug antibiotic resistance in pathogenic bacteria continues to rise, there is a critical need for novel antimicrobial agents. An essential requirement for a useful antibiotic is that it selectively targets bacteria without significant effects on the eukaryotic hosts. Korormicin is an excellent candidate in this respect because it targets a unique respiratory enzyme found only in prokaryotes, the Na+-pumping NADH:quinone oxidoreductase (Na+-NQR). Korormicin is synthesized by some species of the marine bacterium Pseudoalteromonas and is a potent and specific inhibitor of Na+-NQR, an enzyme that is essential for the survival and proliferation of many Gram-negative human pathogens, including Vibrio cholerae and Pseudomonas aeruginosa, among others. Here, we identified how korormicin selectively kills these bacteria. The binding of korormicin to Na+-NQR promotes the formation of reactive oxygen species generated by the reaction of the FAD and the 2Fe-2S center cofactors with O2.

scholarly journals Characterization of theVibrio choleraePhage Shock Protein Response

2019 ◽  
Vol 201 (14) ◽  
Author(s):  
Cara M. DeAngelis ◽  
Dhrubajyoti Nag ◽  
Jeffrey H. Withey ◽  
Jyl S. Matson
Keyword(s):  
Stress Response ◽  
Vibrio Cholerae ◽  
Membrane Damage ◽  
Regulatory Elements ◽  
Life Cycles ◽  
Gram Negative Bacteria ◽  
Gram Negative ◽  
Content Type ◽  
Genetic Components ◽  
Stress Response Pathway

ABSTRACTThe phage shock protein (Psp) system is a stress response pathway that senses and responds to inner membrane damage. The genetic components of the Psp system are present in several clinically relevant Gram-negative bacteria, includingVibrio cholerae. However, most of the current knowledge about the Psp response stems fromin vitrostudies inEscherichia coliandYersinia enterocolitica. In fact, the Psp response inV. choleraehas remained completely uncharacterized. In this study, we demonstrate thatV. choleraedoes have a functional Psp response system. We found that overexpression of GspD (EpsD), the type II secretion system secretin, induces the Psp response, whereas otherV. choleraesecretins do not. In addition, we have identified several environmental conditions that induce this stress response. Our studies on the genetic regulation and induction of the Psp system inV. choleraesuggest that the key regulatory elements are conserved with those of other Gram-negative bacteria. While apspnull strain is fully capable of colonizing the infant mouse intestine, it exhibits a colonization defect in a zebrafish model, indicating that this response may be important for disease transmission in the environment. Overall, these studies provide an initial understanding of a stress response pathway that has not been previously investigated inV. cholerae.IMPORTANCEVibrio choleraeleads a dual life cycle, as it can exist in the aquatic environment and colonize the human small intestine. In both life cycles,V. choleraeencounters a variety of stressful conditions, including fluctuating pH and temperature and exposure to other agents that may negatively affect cell envelope homeostasis. The phage shock protein (Psp) response is required to sense and respond to such insults in other bacteria but has remained unstudied inV. cholerae. Interestingly, the Psp system has protein homologs, principally, PspA, in a number of bacterial clades as well as in archaea and plants. Therefore, our findings not only fill a gap in knowledge about an unstudied extracytoplasmic stress response inV. cholerae, but also may have far-reaching implications.

Cholera

2010 ◽  
pp. 754-759
Author(s):  
Aldo A.M. Lima ◽  
Richard L. Guerrant
Keyword(s):  
Vibrio Cholerae ◽  
Oral Rehydration Therapy ◽  
Developed Countries ◽  
Contaminated Water ◽  
Less Developed Countries ◽  
Gram Negative ◽  
Oral Rehydration ◽  
O Antigen ◽  
Route Of Transmission ◽  
Contaminated Food

Vibrio cholerae is a Gram-negative organism that can be subdivided into over 200 serogroups based on the somatic O antigen, with only serogroups O1 and O139 causing epidemic and pandemic disease. Historically it has killed millions from dehydrating diarrhoea, encouraged the birth of modern epidemiology, the sanitary revolution, and oral rehydration therapy; it persists today as a glaring reminder of poverty and inadequate water/sanitation. Contaminated food (especially undercooked seafood) is the usual route of transmission in developed countries; contaminated water and street food vendors are more common vehicles in less developed countries....

Cholera

2020 ◽  
pp. 1060-1066
Author(s):  
Aldo A.M. Lima ◽  
Richard L. Guerrant
Keyword(s):  
South Asia ◽  
Vibrio Cholerae ◽  
Oral Rehydration Therapy ◽  
Developed Countries ◽  
Contaminated Water ◽  
Gram Negative ◽  
Trade Routes ◽  
Oral Rehydration ◽  
Route Of Transmission ◽  
Contaminated Food

Cholera, the dreaded scourge causing death from dehydrating diarrhoea, existed for centuries in South Asia until, in 1817, it broke out along trade routes; since then there have been seven pandemics across all six inhabited continents. Vibrio cholerae is a Gram-negative organism that can be subdivided into over 200 serogroups based on the somatic O antigen, with only serogroups O1 and O139 causing epidemic and pandemic disease. Historically it has killed millions from dehydrating diarrhoea, encouraged the birth of modern epidemiology, the sanitary revolution, and oral rehydration therapy; it persists today as a glaring reminder of poverty and inadequate water/sanitation. Contaminated food (especially undercooked seafood) is the usual route of transmission in developed countries; contaminated water and street food vendors are more common vehicles in less developed countries.

scholarly journals Genomic and Resistance Epidemiology of Gram-Negative Bacteria in Africa: a Systematic Review and Phylogenomic Analyses from a One Health Perspective

mSystems ◽  
2020 ◽  
Vol 5 (6) ◽  
Author(s):  
John Osei Sekyere ◽  
Melese Abate Reta
Keyword(s):  
Escherichia Coli ◽  
Antibiotic Resistance ◽  
Klebsiella Pneumoniae ◽  
Acinetobacter Baumannii ◽  
Vibrio Cholerae ◽  
Salmonella Enterica ◽  
Animal Health ◽  
Gram Negative Bacteria ◽  
Gram Negative ◽  
Content Type

ABSTRACT Antibiotic resistance (AR) remains a major threat to public and animal health globally. However, AR ramifications in developing countries are worsened by limited molecular diagnostics, expensive therapeutics, inadequate numbers of skilled clinicians and scientists, and unsanitary environments. The epidemiology of Gram-negative bacteria, their AR genes, and geographical distribution in Africa are described here. Data were extracted and analyzed from English-language articles published between 2015 and December 2019. The genomes and AR genes of the various species, obtained from the Pathosystems Resource Integration Center (PATRIC) and NCBI were analyzed phylogenetically using Randomized Axelerated Maximum Likelihood (RAxML) and annotated with Figtree. The geographic location of resistant clones/clades was mapped manually. Thirty species from 31 countries and 24 genera from 41 countries were analyzed from 146 articles and 3,028 genomes, respectively. Genes mediating resistance to β-lactams (including blaTEM-1, blaCTX-M, blaNDM, blaIMP, blaVIM, and blaOXA-48/181), fluoroquinolones (oqxAB, qnrA/B/D/S, gyrA/B, and parCE mutations, etc.), aminoglycosides (including armA and rmtC/F), sulfonamides (sul1/2/3), trimethoprim (dfrA), tetracycline [tet(A/B/C/D/G/O/M/39)], colistin (mcr-1), phenicols (catA/B, cmlA), and fosfomycin (fosA) were mostly found in Enterobacter spp. and Klebsiella pneumoniae, and also in Serratia marcescens, Escherichia coli, Salmonella enterica, Pseudomonas, Acinetobacter baumannii, etc., on mostly IncF-type, IncX3/4, ColRNAI, and IncR plasmids, within IntI1 gene cassettes, insertion sequences, and transposons. Clonal and multiclonal outbreaks and dissemination of resistance genes across species and countries and between humans, animals, plants, and the environment were observed; Escherichia coli ST103, K. pneumoniae ST101, S. enterica ST1/2, and Vibrio cholerae ST69/515 were common strains. Most pathogens were of human origin, and zoonotic transmissions were relatively limited. IMPORTANCE Antibiotic resistance (AR) is one of the major public health threats and challenges to effective containment and treatment of infectious bacterial diseases worldwide. Here, we used different methods to map out the geographical hot spots, sources, and evolutionary epidemiology of AR. Escherichia coli, Klebsiella pneumoniae, Salmonella enterica, Acinetobacter baumannii, Pseudomonas aeruginosa, Enterobacter spp., Neisseria meningitis/gonorrhoeae, Vibrio cholerae, Campylobacter jejuni, etc., were common pathogens shuttling AR genes in Africa. Transmission of the same clones/strains across countries and between animals, humans, plants, and the environment was observed. We recommend Enterobacter spp. or K. pneumoniae as better sentinel species for AR surveillance.

scholarly journals A Transposon Screen Identifies Genetic Determinants of Vibrio cholerae Resistance to High-Molecular-Weight Antibiotics

2016 ◽  
Vol 60 (8) ◽  
pp. 4757-4763 ◽  
Author(s):  
Tobias Dörr ◽  
Fernanda Delgado ◽  
Benjamin D. Umans ◽  
Matthew A. Gerding ◽  
Brigid M. Davis ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Outer Membrane ◽  
Vibrio Cholerae ◽  
High Molecular Weight ◽  
Glycopeptide Antibiotics ◽  
Membrane Function ◽  
General Role ◽  
Gram Negative ◽  
Content Type ◽  
Reading Frame

ABSTRACTGram-negative bacteria are notoriously resistant to a variety of high-molecular-weight antibiotics due to the limited permeability of their outer membrane (OM). The basis of OM barrier function and the genetic factors required for its maintenance remain incompletely understood. Here, we employed transposon insertion sequencing to identify genes required forVibrio choleraeresistance to vancomycin and bacitracin, antibiotics that are thought to be too large to efficiently penetrate the OM. The screen yielded several genes whose protein products are predicted to participate in processes important for OM barrier functions and for biofilm formation. In addition, we identified a novel factor, designatedvigA(for vancomycin inhibits growth), that has not previously been characterized or linked to outer membrane function. ThevigAopen reading frame (ORF) codes for an inner membrane protein, and in its absence, cells became highly sensitive to glycopeptide antibiotics (vancomycin and ramoplanin) and bacitracin but not to other large antibiotics or detergents. In contrast to wild-type (WT) cells, thevigAmutant was stained with fluorescent vancomycin. These observations suggest that VigA specifically prevents the periplasmic accumulation of certain large antibiotics without exerting a general role in the maintenance of OM integrity. We also observed marked interspecies variability in the susceptibilities of Gram-negative pathogens to glycopeptides and bacitracin. Collectively, our findings suggest that the OM barrier is not absolute but rather depends on specific OM-antibiotic interactions.

scholarly journals Host Intestinal Signal-Promoted Biofilm Dispersal Induces Vibrio cholerae Colonization

2014 ◽  
Vol 83 (1) ◽  
pp. 317-323 ◽  
Author(s):  
Amanda J. Hay ◽  
Jun Zhu
Keyword(s):  
Bile Salt ◽  
Vibrio Cholerae ◽  
Diarrheal Disease ◽  
Virulence Gene ◽  
Human Infection ◽  
Content Type ◽  
Abiotic Degradation ◽  
Contaminated Food ◽  
Free Media ◽  
Biofilm Matrix

Vibrio choleraecauses human infection through ingestion of contaminated food and water, leading to the devastating diarrheal disease cholera.V. choleraeforms matrix-encased aggregates, known as biofilms, in the native aquatic environment. While the formation ofV. choleraebiofilms has been well studied, little is known about the dispersal from biofilms, particularly upon entry into the host. In this study, we found that the exposure of mature biofilms to physiologic levels of the bile salt taurocholate, a host signal for the virulence gene induction ofV. cholerae, induces an increase in the number of detached cells with a concomitant decrease in biofilm mass. Scanning electron microscopy micrographs of biofilms exposed to taurocholate revealed an altered, perhaps degraded, appearance of the biofilm matrix. The inhibition of protein synthesis did not alter rates of detachment, suggesting thatV. choleraeundergoes a passive dispersal. Cell-free media from taurocholate-exposed biofilms contains a larger amount of free polysaccharide, suggesting an abiotic degradation of biofilm matrix by taurocholate. Furthermore, we found thatV. choleraeis only able to induce virulence in response to taurocholate after exit from the biofilm. Thus, we propose a model in whichV. choleraeingested as a biofilm has coopted the host-derived bile salt signal to detach from the biofilm and go on to activate virulence.

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