scholarly journals YliH (BssR) and YceP (BssS) Regulate Escherichia coli K-12 Biofilm Formation by Influencing Cell Signaling

2006 ◽  
Vol 72 (4) ◽  
pp. 2449-2459 ◽  
Author(s):  
Joanna Domka ◽  
Jintae Lee ◽  
Thomas K. Wood
Keyword(s):  
Escherichia Coli ◽  
Amino Acids ◽  
Cell Signaling ◽  
Biofilm Formation ◽  
Differentially Expressed ◽  
Wild Type ◽  
Autoinducer 2 ◽  
Expression Of Genes ◽  
Differential Gene ◽  
K 12

ABSTRACT We previously discovered that yliH and yceP are induced in Escherichia coli biofilms (D. Ren, L. A. Bedzyk, S. M. Thomas, R. W. Ye, and T. K. Wood, Appl. Microbiol. Biotechnol. 64:515-524, 2004). Here, it is shown that deletion of yceP (b1060) and yliH (b0836) increases biofilm formation in continuous-flow chambers with minimal glucose medium by increasing biofilm mass (240- to 290-fold), surface coverage (16- to 31-fold), and mean thickness (2,800-fold). To determine the genetic basis of the increase in biofilm formation, we examined the differential gene expression profile in biofilms for both the mutants relative to the wild-type strain in rich medium with glucose and found that 372 to 882 genes were induced and that 76 to 337 were repressed consistently >2-fold (P ≤ 0.05). The increase in biofilm formation was related to differential expression of genes related to stress response (8 to 64 genes) for both mutants, including rpoS and sdiA. More importantly, 42 to 130 genes related to autoinducer 2 cell signaling were also differentially expressed, including gadAB and flgBCEGHIJLMN, as well as signaling through indole, since 17 to 26 indole-related genes were differentially expressed, including phoAER, gltBD, mtr (encodes protein for indole import), and acrEF (encodes proteins for indole export). Increased biofilm formation in the yliH and yceP mutants in LB supplemented with 0.2% glucose (LB glu) occurred through a reduction in extracellular and intracellular indole concentrations in both mutants (50- to 140-fold), and the addition of indole to the culture restored the wild-type biofilm phenotype; hence, indole represses biofilms. Additionally, both mutants regulate biofilms through quorum sensing, since deletion of either yliH or yceP increased extracellular autoinducer 2 concentrations 50-fold when grown in complex medium (most notably in the stationary phase). Both proteins are involved in motility regulation, since YliH (127 amino acids) and YceP (84 amino acids) repressed motility two to sevenfold (P ≤ 0.05) in LB, and YceP repressed motility sevenfold (P ≤ 0.05) in LB glu. Heightened motility in the yceP mutant occurred, due to increased transcription of the flagella and motility loci, including fliC, motA, and qseB (3- to 86-fold). We propose new names for these two loci: bssR for yliH and bssS for yceP, based on the phrase “regulator of biofilm through signal secretion.”

scholarly journals Autoinducer 2 Controls Biofilm Formation in Escherichia coli through a Novel Motility Quorum-Sensing Regulator (MqsR, B3022)

2006 ◽  
Vol 188 (1) ◽  
pp. 305-316 ◽  
Author(s):  
Andrés F. González Barrios ◽  
Rongjun Zuo ◽  
Yoshifumi Hashimoto ◽  
Li Yang ◽  
William E. Bentley ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Quorum Sensing ◽  
Continuous Flow ◽  
Biofilm Formation ◽  
Type Strain ◽  
Wild Type Strain ◽  
Wild Type ◽  
Flow Cells ◽  
Autoinducer 2 ◽  
K 12

ABSTRACT The cross-species bacterial communication signal autoinducer 2 (AI-2), produced by the purified enzymes Pfs (nucleosidase) and LuxS (terminal synthase) from S-adenosylhomocysteine, directly increased Escherichia coli biofilm mass 30-fold. Continuous-flow cells coupled with confocal microscopy corroborated these results by showing the addition of AI-2 significantly increased both biofilm mass and thickness and reduced the interstitial space between microcolonies. As expected, the addition of AI-2 to cells which lack the ability to transport AI-2 (lsr null mutant) failed to stimulate biofilm formation. Since the addition of AI-2 increased cell motility through enhanced transcription of five motility genes, we propose that AI-2 stimulates biofilm formation and alters its architecture by stimulating flagellar motion and motility. It was also found that the uncharacterized protein B3022 regulates this AI-2-mediated motility and biofilm phenotype through the two-component motility regulatory system QseBC. Deletion of b3022 abolished motility, which was restored by expressing b3022 in trans. Deletion of b3022 also decreased biofilm formation significantly, relative to the wild-type strain in three media (46 to 74%) in 96-well plates, as well as decreased biomass (8-fold) and substratum coverage (19-fold) in continuous-flow cells with minimal medium (growth rate not altered and biofilm restored by expressing b3022 in trans). Deleting b3022 changed the wild-type biofilm architecture from a thick (54-μm) complex structure to one that contained only a few microcolonies. B3022 positively regulates expression of qseBC, flhD, fliA, and motA, since deleting b3022 decreased their transcription by 61-, 25-, 2.4-, and 18-fold, respectively. Transcriptome analysis also revealed that B3022 induces crl (26-fold) and flhCD (8- to 27-fold). Adding AI-2 (6.4 μM) increased biofilm formation of wild-type K-12 MG1655 but not that of the isogenic b3022, qseBC, fliA, and motA mutants. Adding AI-2 also increased motA transcription for the wild-type strain but did not stimulate motA transcription for the b3022 and qseB mutants. Together, these results indicate AI-2 induces biofilm formation in E. coli through B3022, which then regulates QseBC and motility; hence, b3022 has been renamed the motility quorum-sensing regulator gene (the mqsR gene).

scholarly journals YdgG (TqsA) Controls Biofilm Formation in Escherichia coli K-12 through Autoinducer 2 Transport

2006 ◽  
Vol 188 (2) ◽  
pp. 587-598 ◽  
Author(s):  
Moshe Herzberg ◽  
Ian K. Kaye ◽  
Wolfgang Peti ◽  
Thomas K. Wood
Keyword(s):  
Escherichia Coli ◽  
Biofilm Formation ◽  
Acid Production ◽  
Polysialic Acid ◽  
Fold Increase ◽  
Uncharacterized Protein ◽  
Biofilm Thickness ◽  
Autoinducer 2 ◽  
Membrane Spanning ◽  
K 12

ABSTRACT YdgG is an uncharacterized protein that is induced in Escherichia coli biofilms. Here it is shown that deletion of ydgG decreased extracellular and increased intracellular concentrations of autoinducer 2 (AI-2); hence, YdgG enhances transport of AI-2. Consistent with this hypothesis, deletion of ydgG resulted in a 7,000-fold increase in biofilm thickness and 574-fold increase in biomass in flow cells. Also consistent with the hypothesis, deletion of ydgG increased cell motility by increasing transcription of flagellar genes (genes induced by AI-2). By expressing ydgG in trans, the wild-type phenotypes for extracellular AI-2 activity, motility, and biofilm formation were restored. YdgG is also predicted to be a membrane-spanning protein that is conserved in many bacteria, and it influences resistance to several antimicrobials, including crystal violet and streptomycin (this phenotype could also be complemented). Deletion of ydgG also caused 31% of the bacterial chromosome to be differentially expressed in biofilms, as expected, since AI-2 controls hundreds of genes. YdgG was found to negatively modulate expression of flagellum- and motility-related genes, as well as other known products essential for biofilm formation, including operons for type 1 fimbriae, autotransporter protein Ag43, curli production, colanic acid production, and production of polysaccharide adhesin. Eighty genes not previously related to biofilm formation were also identified, including those that encode transport proteins (yihN and yihP), polysialic acid production (gutM and gutQ), CP4-57 prophage functions (yfjR and alpA), methionine biosynthesis (metR), biotin and thiamine biosynthesis (bioF and thiDFH), anaerobic metabolism (focB, hyfACDR, ttdA, and fumB), and proteins with unknown function (ybfG, yceO, yjhQ, and yjbE); 10 of these genes were verified through mutation to decrease biofilm formation by 40% or more (yfjR, bioF, yccW, yjbE, yceO, ttdA, fumB, yjiP, gutQ, and yihR). Hence, it appears YdgG controls the transport of the quorum-sensing signal AI-2, and so we suggest the gene name tqsA.

scholarly journals The Transcriptional Antiterminator RfaH Represses Biofilm Formation in Escherichia coli

2006 ◽  
Vol 188 (4) ◽  
pp. 1316-1331 ◽  
Author(s):  
Christophe Beloin ◽  
Kai Michaelis ◽  
Karin Lindner ◽  
Paolo Landini ◽  
Jörg Hacker ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Biofilm Formation ◽  
Wild Type Strain ◽  
Wild Type ◽  
Strain Mg1655 ◽  
Upec Strain ◽  
E Coli ◽  
Initial Adhesion ◽  
State Production ◽  
K 12

ABSTRACT We investigated the influence of regulatory and pathogenicity island-associated factors (Hha, RpoS, LuxS, EvgA, RfaH, and tRNA5 Leu) on biofilm formation by uropathogenic Escherichia coli (UPEC) strain 536. Only inactivation of rfaH, which encodes a transcriptional antiterminator, resulted in increased initial adhesion and biofilm formation by E. coli 536. rfaH inactivation in nonpathogenic E. coli K-12 isolate MG1655 resulted in the same phenotype. Transcriptome analysis of wild-type strain 536 and an rfaH mutant of this strain revealed that deletion of rfaH correlated with increased expression of flu orthologs. flu encodes antigen 43 (Ag43), which mediates autoaggregation and biofilm formation. We confirmed that deletion of rfaH leads to increased levels of flu and flu-like transcripts in E. coli K-12 and UPEC. Supporting the hypothesis that RfaH represses biofilm formation through reduction of the Ag43 level, the increased-biofilm phenotype of E. coli MG1655rfaH was reversed upon inactivation of flu. Deletion of the two flu orthologs, however, did not modify the behavior of mutant 536rfaH. Our results demonstrate that the strong initial adhesion and biofilm formation capacities of strain MG1655rfaH are mediated by both increased steady-state production of Ag43 and likely increased Ag43 presentation due to null rfaH-dependent lipopolysaccharide depletion. Although the roles of rfaH in the biofilm phenotype are different in UPEC strain 536 and K-12 strain MG1655, this study shows that RfaH, in addition to affecting the expression of bacterial virulence factors, also negatively controls expression and surface presentation of Ag43 and possibly another Ag43-independent factor(s) that mediates cell-cell interactions and biofilm formation.

Identification of Ground Beef–Derived Fatty Acid Inhibitors of Autoinducer-2–Based Cell Signaling

2008 ◽  
Vol 71 (1) ◽  
pp. 134-138 ◽  
Author(s):  
KAMLESH A. SONI ◽  
PALMY JESUDHASAN ◽  
MARTHA CEPEDA ◽  
KENNETH WIDMER ◽  
G. K. JAYAPRAKASHA ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Cell Signaling ◽  
Biofilm Formation ◽  
Ground Beef ◽  
Acid Mixture ◽  
Autoinducer 2 ◽  
Beef Extract ◽  
Reporter Strains ◽  
K 12

Autoinducer-2 (AI-2) molecules are used by several microorganisms to modulate various processes, including bioluminescence, biofilm formation, and virulence expression. Certain food matrices, including ground beef extracts, possess compounds capable of inhibiting AI-2 activity. In the present study, we identified and characterized these AI-2 inhibitors from ground beef extract using hexane solvent extraction and gas chromatography. Gas chromatographic analysis revealed the presence of several fatty acids such as palmitic acid (C16:0), stearic acid (C18:0), oleic acid (C18:1ω9), and linoleic acid (C18:2ω6) that were capable of inhibiting AI-2 activity. These fatty acids were tested (using Vibrio harveyi BB170 and MM32 reporter strains) at different concentrations (1, 5, and 10 mM) to identify differences in the level of AI-2 activity inhibition. AI-2 inhibition ranged from 25 to 90%. A mixture of these fatty acids (prepared at concentrations equivalent to those present in the ground beef extract) produced 52 to 65% inhibition of AI-2 activity. The fatty acid mixture also negatively influenced Escherichia coli K-12 biofilm formation. These results demonstrate that both medium- and long-chain fatty acids in ground beef have the ability to interfere with AI-2–based cell signaling.

scholarly journals Regulation ofwaaHby PhoB during PiStarvation Promotes Biofilm Formation byEscherichia coliO157:H7

2019 ◽  
Vol 201 (18) ◽  
Author(s):  
Philippe Vogeleer ◽  
Antony T. Vincent ◽  
Samuel M. Chekabab ◽  
Steve J. Charette ◽  
Alexey Novikov ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Biofilm Formation ◽  
Ecological Niches ◽  
Pho Regulon ◽  
Starvation Stress ◽  
Content Type ◽  
E Coli ◽  
Expression Of Genes ◽  
K 12 ◽  
Pst System

ABSTRACTIn open environments such as water, enterohemorrhagicEscherichia coliO157:H7 responds to inorganic phosphate (Pi) starvation by inducing the Pho regulon controlled by PhoB. This activates the phosphate-specific transport (Pst) system that contains a high-affinity Pitransporter. In the Δpstmutant, PhoB is constitutively activated and regulates the expression of genes in the Pho regulon. Here, we show that Pistarvation and deletion of thepstsystem enhanceE. coliO157:H7 biofilm formation. Among differentially expressed genes of EDL933 grown under Pistarvation conditions and in the Δpstmutant, we have found that a member of the PhoB regulon,waaH, predicted to encode a glycosyltransferase, was highly expressed. Interestingly, WaaH contributed to biofilm formation ofE. coliO157:H7 during both Pistarvation and in the Δpstmutant. In the Δpstmutant, the presence ofwaaHwas associated with lipopolysaccharide (LPS) R3 core type modifications, whereas inE. coliO157:H7,waaHoverexpression had no effect on LPS structure during Pistarvation. Therefore,waaHparticipates inE. coliO157:H7 biofilm formation during Pistarvation, but its biochemical role remains to be clarified. This study highlights the importance of the Pistarvation stress response to biofilm formation, which may contribute to the persistence ofE. coliO157:H7 in the environment.IMPORTANCEEnterohemorrhagicEscherichia coliO157:H7 is a human pathogen that causes bloody diarrhea that can result in renal failure. Outside of mammalian hosts,E. coliO157:H7 survives for extended periods of time in nutrient-poor environments, likely as part of biofilms. InE. coliK-12, the levels of free extracellular Piaffect biofilm formation; however, it was unknown whether Piinfluences biofilm formation byE. coliO157:H7. Our results show that upon Pistarvation, PhoB activateswaaHexpression, which favors biofilm formation byE. coliO157:H7. These findings suggest that WaaH is a target for controlling biofilm formation. Altogether, our work demonstrates how adaptation to Pistarvation allowsE. coliO157:H7 to occupy different ecological niches.

scholarly journals Overexpression ofluxSCannot Increase Autoinducer-2 Production, Only Affect the Growth and Biofilm Formation inStreptococcus suis

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Yang Wang ◽  
Li Yi ◽  
Zhicheng Zhang ◽  
Hongjie Fan ◽  
Xiangchao Cheng ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Cell Signaling ◽  
Host Cell ◽  
Growth Phase ◽  
Biofilm Formation ◽  
Mutant Gene ◽  
Wild Type ◽  
Cell Adherence ◽  
Phase Dependence ◽  
Autoinducer 2

LuxS/AI-2 quorum sensing (QS) system involves the production of cell signaling molecules vialuxS-based autoinducer-2 (AI-2). LuxS has been reported to plays critical roles in regulating various behaviors of bacteria. AI-2 is a byproduct of the catabolism of S-adenosylhomocysteine (SAH) performed by the LuxS and Pfs enzymes. In our previous study, the function of LuxS in AI-2 production was verified inStreptococcus suis(SS). Decreased levels of SS biofilm formation and host-cell adherence as well as an inability to produce AI-2 were observed in bacteria having aluxSmutant gene. In this study, the level of AI-2 activity exhibits a growth-phase dependence with a maximum in late exponential culture in SS. An SS strain that overexpressedluxSwas constructed to comprehensively understand the function of AI-2. OverexpressedluxSwas not able to increase the level ofpfsexpression and produce additional AI-2, and the bacteria were slower growing and produced only slightly more biofilm than the wild type. Thus, AI-2 production is not correlated withluxStranscription.luxSexpression is constitutive, but the transcription ofpfsis perhaps correlated with AI-2 production in SS.

scholarly journals Role of DLP12 lysis genes in Escherichia coli biofilm formation

Microbiology ◽  
2011 ◽  
Vol 157 (6) ◽  
pp. 1640-1650 ◽  
Author(s):  
Faustino A. Toba ◽  
Mitchell G. Thompson ◽  
Bryan R. Campbell ◽  
Lauren M. Junker ◽  
Karl-Gustav Rueggeberg ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Wall ◽  
Biofilm Formation ◽  
Wall Stress ◽  
Wild Type ◽  
Lambda Phage ◽  
Kinase Gene ◽  
Abiotic Surfaces ◽  
K 12 ◽  
Biofilm Development

Phages have recently been implicated as important in biofilm development, although the mechanisms whereby phages impact biofilms remain unclear. One defective lambdoid phage carried by Escherichia coli K-12 is DLP12. Among the genes found in DLP12 are essD, ybcS and rzpD/rzoD, which are homologues of the Lambda phage genes encoding cell-lysis proteins (S, R and Rz/Rz1). The role that these DLP12 lysis genes play in biofilm formation was examined in deletion mutants of E. coli PHL628, a curli-overproducing, biofilm-forming K-12 derivative. Strains lacking essD, ybcS and rzpD/rzoD were unable to form wild-type biofilms. While all mutants were compromised in attachment to abiotic surfaces and aggregated less well than the wild-type, the effect of the essD knockout on biofilm formation was less dramatic than that of deleting ybcS or rzpD/rzoD. These results were consistent with electron micrographs of the mutants, which showed a decreased number of curli fibres on cell surfaces. Also consistent with this finding, we observed that expression from the promoter of csgB, which encodes the curli subunits, was downregulated in the mutants. As curli production is transcriptionally downregulated in response to cell wall stress, we challenged the mutants with SDS and found them to be more sensitive to the detergent than the wild-type. We also examined the release of 14C-labelled peptidoglycan from the mutants and found that they did not lose labelled peptidoglycan to the same extent as the wild-type. Given that curli production is known to be suppressed by N-acetylglucosamine 6-phosphate (NAG-6P), a metabolite produced during peptidoglycan recycling, we deleted nagK, the N-acetylglucosamine kinase gene, from the lysis mutants and found that this restored curli production. This suggested that deletion of the lysis genes affected cell wall status, which was transduced to the curli operon by NAG-6P via an as yet unknown mechanism. These observations provide evidence that the S, R and Rz/Rz1 gene homologues encoded by DLP12 are not merely genetic junk, but rather play an important, though undefined, role in cell wall maintenance.

scholarly journals Differential Effects of Epinephrine, Norepinephrine, and Indole on Escherichia coli O157:H7 Chemotaxis, Colonization, and Gene Expression

2007 ◽  
Vol 75 (9) ◽  
pp. 4597-4607 ◽  
Author(s):  
Tarun Bansal ◽  
Derek Englert ◽  
Jintae Lee ◽  
Manjunath Hegde ◽  
Thomas K. Wood ◽  
...  
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Biofilm Formation ◽  
Signaling Molecules ◽  
Signal Molecules ◽  
Autoinducer 2 ◽  
Expression Of Genes ◽  
Wide Range ◽  
Host Cell Surface

ABSTRACT During infection in the gastrointestinal tract, enterohemorrhagic Escherichia coli (EHEC) O157:H7 is exposed to a wide range of signaling molecules, including the eukaryotic hormones epinephrine and norepinephrine, and bacterial signal molecules such as indole. Since these signaling molecules have been shown to be involved in the regulation of phenotypes such as motility and virulence that are crucial for EHEC infections, we hypothesized that these molecules also govern the initial recognition of the large intestine environment and attachment to the host cell surface. Here, we report that, compared to indole, epinephrine and norepinephrine exert divergent effects on EHEC chemotaxis, motility, biofilm formation, gene expression, and colonization of HeLa cells. Using a novel two-fluorophore chemotaxis assay, it was found that EHEC is attracted to epinephrine and norepinephrine while it is repelled by indole. In addition, epinephrine and norepinephrine also increased EHEC motility and biofilm formation while indole attenuated these phenotypes. DNA microarray analysis of surface-associated EHEC indicated that epinephrine/norepinephrine up-regulated the expression of genes involved in surface colonization and virulence while exposure to indole decreased their expression. The gene expression data also suggested that autoinducer 2 uptake was repressed upon exposure to epinephrine/norepinephrine but not indole. In vitro adherence experiments confirmed that epinephrine and norepinephrine increased attachment to epithelial cells while indole decreased adherence. Taken together, these results suggest that epinephrine and norepinephrine increase EHEC infection while indole attenuates the process.

scholarly journals Deletion of the yiaMNO transporter genes affects the growth characteristics of Escherichia coli K-12

Microbiology ◽  
2005 ◽  
Vol 151 (5) ◽  
pp. 1683-1689 ◽  
Author(s):  
Titia H. Plantinga ◽  
Chris van der Does ◽  
Danuta Tomkiewicz ◽  
Geertje van Keulen ◽  
Wil N. Konings ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Biofilm Formation ◽  
Sole Carbon Source ◽  
Binding Protein ◽  
Physiological Role ◽  
Proton Motive Force ◽  
Growth Characteristics ◽  
Wild Type ◽  
E Coli ◽  
K 12

Binding-protein-dependent secondary transporters make up a unique transport protein family. They use a solute-binding protein in proton-motive-force-driven transport. Only a few systems have been functionally analysed. The yiaMNO genes of Escherichia coli K-12 encode one family member that transports the rare pentose l-xylulose. Its physiological role is unknown, since wild-type E. coli K-12 does not utilize l-xylulose as sole carbon source. Deletion of the yiaMNO genes in E. coli K-12 strain MC4100 resulted in remarkable changes in the transition from exponential growth to the stationary phase, high-salt survival and biofilm formation.

scholarly journals Differential Gene Expression for Investigation of Escherichia coli Biofilm Inhibition by Plant Extract Ursolic Acid

2005 ◽  
Vol 71 (7) ◽  
pp. 4022-4034 ◽  
Author(s):  
Dacheng Ren ◽  
Rongjun Zuo ◽  
Andrés F. González Barrios ◽  
Laura A. Bedzyk ◽  
Gary R. Eldridge ◽  
...  
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Differential Gene Expression ◽  
Ursolic Acid ◽  
Biofilm Formation ◽  
Minimal Medium ◽  
Sulfur Metabolism ◽  
E Coli ◽  
Differential Gene ◽  
K 12

ABSTRACT After 13,000 samples of compounds purified from plants were screened, a new biofilm inhibitor, ursolic acid, has been discovered and identified. Using both 96-well microtiter plates and a continuous flow chamber with COMSTAT analysis, 10 μg of ursolic acid/ml inhibited Escherichia coli biofilm formation 6- to 20-fold when added upon inoculation and when added to a 24-h biofilm; however, ursolic acid was not toxic to E. coli, Pseudomonas aeruginosa, Vibrio harveyi, and hepatocytes. Similarly, 10 μg of ursolic acid/ml inhibited biofilm formation by >87% for P. aeruginosa in both complex and minimal medium and by 57% for V. harveyi in minimal medium. To investigate the mechanism of this nontoxic inhibition on a global genetic basis, DNA microarrays were used to study the gene expression profiles of E. coli K-12 grown with or without ursolic acid. Ursolic acid at 10 and 30 μg/ml induced significantly (P < 0.05) 32 and 61 genes, respectively, and 19 genes were consistently induced. The consistently induced genes have functions for chemotaxis and mobility (cheA, tap, tar, and motAB), heat shock response (hslSTV and mopAB), and unknown functions (such as b1566 and yrfHI). There were 31 and 17 genes repressed by 10 and 30 μg of ursolic acid/ml, respectively, and 12 genes were consistently repressed that have functions in cysteine synthesis (cysK) and sulfur metabolism (cysD), as well as unknown functions (such as hdeAB and yhaDFG). Ursolic acid inhibited biofilms without interfering with quorum sensing, as shown with the V. harveyi AI-1 and AI-2 reporter systems. As predicted by the differential gene expression, deleting motAB counteracts ursolic acid inhibition (the paralyzed cells no longer become too motile). Based on the differential gene expression, it was also discovered that sulfur metabolism (through cysB) affects biofilm formation (in the absence of ursolic acid).

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