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Role of a GntR-family response regulator LbrA in Listeria monocytogenes biofilm formation.

ABSTRACT: The formation of Listeria monocytogenes biofilms contributes to persistent contamination in food processing facilities. A microarray comparison of L. monocytogenes between the transcriptome of the strong biofilm forming strain (Bfm(s)) Scott A and the weak biofilm forming (Bfm(w)) strain F2365 was conducted to identify genes potentially involved in biofilm formation. Among 951 genes with significant difference in expression between the two strains, a GntR-family response regulator encoding gene (LMOf2365_0414), designated lbrA, was found to be highly expressed in Scott A relative to F2365. A Scott A lbrA-deletion mutant, designated AW3, formed biofilm to a much lesser extent as compared to the parent strain by a rapid attachment assay and scanning electron microscopy. Complementation with lbrA from Scott A restored the Bfm(s) phenotype in the AW3 derivative. A second microarray assessment using the lbrA deletion mutant AW3 and the wild type Scott A revealed a total of 304 genes with expression significantly different between the two strains, indicating the potential regulatory role of LbrA in L. monocytogenes. A cloned copy of Scott A lbrA was unable to confer enhanced biofilm forming potential in F2365, suggesting that additional factors contributed to weak biofilm formation by F2365.

SUBMITTER: Wassinger A

PROVIDER: S-EPMC3720924 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Role of a GntR-family response regulator LbrA in Listeria monocytogenes biofilm formation

Project description:The formation of Listeria monocytogenes biofilms contributes to persistent contamination in food processing facilities. A microarray comparison of L. monocytogenes between the transcriptome of the strong biofilm forming strain (Bfms) Scott A and the weak biofilm forming (Bfmw) strain F2365 was conducted to identify genes potentially involved in biofilm formation. Among 951 genes with significant difference in expression between the two strains, a GntR-family response regulator encoding gene (LMOf2365_0414), designated lbrA, was found to be highly expressed in Scott A relative to F2365. A Scott A lbrA-deletion mutant, designated AW3, formed biofilm to a much lesser extent as compared to the parent strain by a rapid attachment assay and scanning electron microscopy. Complementation with lbrA from Scott A restored the Bfms phenotype in the AW3 derivative. A second microarray assessment using the lbrA deletion mutant AW3 and the wild type Scott A revealed a total of 304 genes with expression significantly different between the two strains, indicating the potential regulatory role of LbrA in L. monocytogenes. A cloned copy of Scott A lbrA was unable to confer enhanced biofilm forming potential in F2365, suggesting that additional factors contributed to weak biofilm formation by F2365. Findings from the study may lead to new strategies to modulate biofilm formation.

2012-09-06 | GSE40598 | GEO

Role of a GntR-family response regulator LbrA in Listeria monocytogenes biofilm formation

2012-09-06 | E-GEOD-40598 | biostudies-arrayexpress

The virulence regulator PrfA promotes biofilm formation by Listeria monocytogenes.

Project description:Listeria monocytogenes is a food-borne facultative intracellular pathogen. It is widespread in the environment and has several distinct life-styles. The key transcriptional activator PrfA positively regulates L. monocytogenes virulence genes to mediate the transition from extracellular, flagellum-propelled cell to intracellular pathogen. Here we report the first evidence that PrfA also has a significant positive impact on extracellular biofilm formation. Mutants lacking prfA were defective in surface-adhered biofilm formation. The DeltaprfA mutant exhibited wild-type flagellar motility, and its biofilm defect occurred after initial surface adhesion. We also observed that mutations that led to the constitutive expression of PrfA-dependent virulence genes had a minimal impact on biofilm formation. Furthermore, biofilm development was enhanced in a mutant encoding a PrfA protein variant unable to fully transition from the extracellular form to the virulent, intracellular activity conformation. These results indicate that PrfA positively regulates biofilm formation and suggest that PrfA has a global role in modulating the life-style of L. monocytogenes. The requirement of PrfA for optimal biofilm formation may provide selective pressure to maintain this critical virulence regulator when L. monocytogenes is outside host cells in the environment.

| S-EPMC2916369 | biostudies-literature

Role of extracellular DNA during biofilm formation by Listeria monocytogenes.

Project description:Listeria monocytogenes is a food-borne pathogen that is capable of living in harsh environments. It is believed to do this by forming biofilms, which are surface-associated multicellular structures encased in a self-produced matrix. In this paper we show that in L. monocytogenes extracellular DNA (eDNA) may be the only central component of the biofilm matrix and that it is necessary for both initial attachment and early biofilm formation for 41 L. monocytogenes strains that were tested. DNase I treatment resulted in dispersal of biofilms, not only in microtiter tray assays but also in flow cell biofilm assays. However, it was also demonstrated that in a culture without eDNA, neither Listeria genomic DNA nor salmon sperm DNA by itself could restore the capacity to adhere. A search for additional necessary components revealed that peptidoglycan (PG), specifically N-acetylglucosamine (NAG), interacted with the DNA in a manner which restored adhesion. If a short DNA fragment (less than approximately 500 bp long) was added to an eDNA-free culture prior to addition of genomic or salmon sperm DNA, adhesion was prevented, indicating that high-molecular-weight DNA is required for adhesion and that the number of attachment sites on the cell surface can be saturated.

| S-EPMC2849236 | biostudies-literature

The role of the Listeria monocytogenes surfactome in biofilm formation.

Project description:Listeria monocytogenes is a highly pathogenic foodborne bacterium that is ubiquitous in the natural environment and capable of forming persistent biofilms in food processing environments. This species has a rich repertoire of surface structures that enable it to survive, adapt and persist in various environments and promote biofilm formation. We review current understanding and advances on how L. monocytogenes organizes its surface for biofilm formation on surfaces associated with food processing settings, because they may be an important target for development of novel antibiofilm compounds. A synthesis of the current knowledge on the role of Listeria surfactome, comprising peptidoglycan, teichoic acids and cell wall proteins, during biofilm formation on abiotic surfaces is provided. We consider indications gained from genome-wide studies and discuss surfactome structures with established mechanistic aspects in biofilm formation. Additionally, we look at the analogies to the species L. innocua, which is closely related to L. monocytogenes and often used as its model (surrogate) organism.

| S-EPMC8313260 | biostudies-literature

Role of SigB in Listeria monocytogenes biofilm formation

Project description:Exploiting genomic differences between Listeria monocytogenes EGDe isolates reveals crucial roles for SigB and wall rhamnosylation in biofilm formation.

2019-11-18 | PRJEB35335 | EVA

Efficacy of Synthetic Furanones on Listeria monocytogenes Biofilm Formation.

Project description:Furanones are analogues of acylated homoserine lactones with proven antifouling activity in both Gram-positive and Gram-negative bacteria though the interference of various quorum sensing pathways. In an attempt to find new strategies to prevent and control Listeria monocytogenes biofilm formation on stainless steel (SS) surfaces, different concentrations of six synthetic furanones were applied on biofilms formed by strains isolated from food, environmental, and clinical sources grown onto AISI 316 SS coupons. Among the furanones tested, (Z-)-4-Bromo-5-(bromomethylene)-2(5H)-furanone and 3,4-Dichloro-2(5H)-furanone significantly (p < 0.05) reduced the adhesion capacity (>1 log CFU cm-2) in 24 h treated biofilms. Moreover, individually conducted experiments demonstrated that (Z-)-4-Bromo-5-(bromomethylene)-2(5H)-furanone was able to not only significantly (p < 0.05) prevent L. monocytogenes adhesion but also to reduce the growth rate of planktonic cells up to 48 h in a dose-dependent manner. LIVE/DEAD staining followed by epifluorescence microscopy visualisation confirmed these results show an alteration of the structure of the biofilm in furanone-treated samples. Additionally, it was demonstrated that 20 µmol L-1 of 3,4-Dichloro-2(5H)-furanone dosed at 0, 24 and 96 h was able to maintain a lower level of adhered cells (>1 log CFU cm-2; p < 0.05). Since furanones do not pose a selective pressure on bacteria, these results represent an appealing novel strategy for the prevention of L. monocytogenes biofilm grown onto SS.

| S-EPMC6963563 | biostudies-literature

Identification of Listeria monocytogenes determinants required for biofilm formation.

Project description:Listeria monocytogenes is a Gram-positive, food-borne pathogen of humans and animals. L. monocytogenes is considered to be a potential public health risk by the U.S. Food and Drug Administration (FDA), as this bacterium can easily contaminate ready-to-eat (RTE) foods and cause an invasive, life-threatening disease (listeriosis). Bacteria can adhere and grow on multiple surfaces and persist within biofilms in food processing plants, providing resistance to sanitizers and other antimicrobial agents. While whole genome sequencing has led to the identification of biofilm synthesis gene clusters in many bacterial species, bioinformatics has not identified the biofilm synthesis genes within the L. monocytogenes genome. To identify genes necessary for L. monocytogenes biofilm formation, we performed a transposon mutagenesis library screen using a recently constructed Himar1 mariner transposon. Approximately 10,000 transposon mutants within L. monocytogenes strain 10403S were screened for biofilm formation in 96-well polyvinyl chloride (PVC) microtiter plates with 70 Himar1 insertion mutants identified that produced significantly less biofilms. DNA sequencing of the transposon insertion sites within the isolated mutants revealed transposon insertions within 38 distinct genetic loci. The identification of mutants bearing insertions within several flagellar motility genes previously known to be required for the initial stages of biofilm formation validated the ability of the mutagenesis screen to identify L. monocytogenes biofilm-defective mutants. Two newly identified genetic loci, dltABCD and phoPR, were selected for deletion analysis and both ΔdltABCD and ΔphoPR bacterial strains displayed biofilm formation defects in the PVC microtiter plate assay, confirming these loci contribute to biofilm formation by L. monocytogenes.

| S-EPMC4269431 | biostudies-literature

Role of PBPD1 in stimulation of Listeria monocytogenes biofilm formation by subminimal inhibitory β-lactam concentrations.

Project description:Disinfectant-tolerant Listeria monocytogenes biofilms can colonize surfaces that come into contact with food, leading to contamination and, potentially, food-borne illnesses. To better understand the process of L. monocytogenes biofilm formation and dispersal, we screened 1,120 off-patent FDA-approved drugs and identified several that modulate Listeria biofilm development. Among the hits were more than 30 β-lactam antibiotics, with effects ranging from inhibiting (≤50%) to stimulating (≥200%) biofilm formation compared to control. Most β-lactams also dispersed a substantial proportion of established biofilms. This phenotype did not necessarily involve killing, as >50% dispersal could be achieved with concentrations as low as 1/20 of the MIC of some cephalosporins. Penicillin-binding protein (PBP) profiling using a fluorescent penicillin analogue showed similar inhibition patterns for most β-lactams, except that biofilm-stimulatory drugs did not bind PBPD1, a low-molecular-weight d,d-carboxypeptidase. Compared to the wild type, a pbpD1 mutant had an attenuated biofilm response to stimulatory β-lactams. The cephalosporin-responsive CesRK two-component regulatory system, whose regulon includes PBPs, was not required for the response. The requirement for PBPD1 activity for β-lactam stimulation of L. monocytogenes biofilms shows that the specific set of PBPs that are inactivated by a particular drug dictates whether a protective biofilm response is provoked.

| S-EPMC4249420 | biostudies-literature

A Mutation in the luxS gene influences Listeria monocytogenes biofilm formation.

Project description:Using a Vibrio harveyi reporter strain, we demonstrated that Listeria monocytogenes secretes a functional autoinducer 2 (AI-2)-like signal. A luxS-deficient mutant produced a denser biofilm and attached to a glass surface 19-fold better than the parent strain. Exogenous AI-2 failed to restore the wild-type phenotype to the mutant. It seems that an intact luxS gene is associated with repression of components required for attachment and biofilm formation.

| S-EPMC1538747 | biostudies-literature

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