scholarly journals Identification of signaling pathways, matrix-digestion enzymes, and motility components controllingVibrio choleraebiofilm dispersal

2020 ◽  
Vol 117 (51) ◽  
pp. 32639-32647
Author(s):  
Andrew A. Bridges ◽  
Chenyi Fei ◽  
Bonnie L. Bassler
Keyword(s):  
Disease Transmission ◽  
Biofilm Formation ◽  
Cell Attachment ◽  
Sensory System ◽  
Signaling Proteins ◽  
Matrix Degradation ◽  
Three Stages ◽  
Matrix Production ◽  
Biofilm Dispersal ◽  
Signal Transduction Proteins

Bacteria alternate between being free-swimming and existing as members of sessile multicellular communities called biofilms. The biofilm lifecycle occurs in three stages: cell attachment, biofilm maturation, and biofilm dispersal.Vibrio choleraebiofilms are hyperinfectious, and biofilm formation and dispersal are considered central to disease transmission. While biofilm formation is well studied, almost nothing is known about biofilm dispersal. Here, we conducted an imaging screen forV. choleraemutants that fail to disperse, revealing three classes of dispersal components: signal transduction proteins, matrix-degradation enzymes, and motility factors. Signaling proteins dominated the screen and among them, we focused on an uncharacterized two-component sensory system that we term DbfS/DbfR for dispersal of biofilm sensor/regulator. Phospho-DbfR represses biofilm dispersal. DbfS dephosphorylates and thereby inactivates DbfR, which permits dispersal. Matrix degradation requires two enzymes: LapG, which cleaves adhesins, and RbmB, which digests matrix polysaccharides. Reorientation in swimming direction, mediated by CheY3, is necessary for cells to escape from the porous biofilm matrix. We suggest that these components act sequentially: signaling launches dispersal by terminating matrix production and triggering matrix digestion, and subsequent cell motility permits escape from biofilms. This study lays the groundwork for interventions aimed at modulatingV. choleraebiofilm dispersal to ameliorate disease.

scholarly journals Identification and analysis of the signaling pathways, matrix-digestion enzymes, and motility components controlling Vibrio cholerae biofilm dispersal

2020 ◽  
Author(s):  
Andrew Bridges ◽  
Chenyi Fei ◽  
Bonnie Bassler
Keyword(s):  
Vibrio Cholerae ◽  
Disease Transmission ◽  
Biofilm Formation ◽  
Cell Attachment ◽  
Sensory System ◽  
Signaling Proteins ◽  
Matrix Degradation ◽  
Three Stages ◽  
Biofilm Dispersal ◽  
Signal Transduction Proteins

Abstract Bacteria alternate between being free-swimming and existing as members of sessile multicellular communities called biofilms. The biofilm lifecycle occurs in three stages: cell attachment, biofilm maturation, and biofilm dispersal. Vibrio cholerae biofilms are hyper-infectious and biofilm formation and dispersal are considered central to disease transmission. While biofilm formation is well-studied, almost nothing is known about biofilm dispersal. Here, we conduct an imaging screen for V. cholerae mutants that fail to disperse, revealing three classes of dispersal components: signal transduction proteins, matrix-degradation enzymes, and motility factors. Signaling proteins dominated the screen and among them, we focused on an uncharacterized two-component sensory system that we name DbfS/DbfR for Dispersal of Biofilm Sensor/Regulator. Phospho-DbfR represses biofilm dispersal. DbfS dephosphorylates and thereby inactivates DbfR, which permits dispersal. Matrix degradation requires two enzymes: LapG, which cleaves adhesins, and RbmB, which digests matrix polysaccharide. Reorientations in swimming direction, mediated by CheY3, are necessary for cells to escape from the porous biofilm matrix. We suggest that these components act sequentially: signaling launches dispersal by terminating matrix production and triggering matrix digestion and, subsequently, cell motility permits escape from biofilms. This study lays the groundwork for interventions that modulate V. cholerae biofilm dispersal to ameliorate disease.

scholarly journals Identification of signaling pathways, matrix-digestion enzymes, and motility components controlling Vibrio cholerae biofilm dispersal

2020 ◽  
Author(s):  
Andrew A. Bridges ◽  
Chenyi Fei ◽  
Bonnie L. Bassler
Keyword(s):  
Signal Transduction ◽  
Vibrio Cholerae ◽  
Disease Transmission ◽  
Biofilm Formation ◽  
Cell Attachment ◽  
Sensory System ◽  
Matrix Degradation ◽  
Free Swimming ◽  
Molecular Events ◽  
Biofilm Dispersal

AbstractBacteria alternate between being free-swimming and existing as members of sessile multicellular communities called biofilms. The biofilm lifecycle occurs in three stages: cell attachment, biofilm maturation, and biofilm dispersal. Vibrio cholerae biofilms are hyper-infectious and biofilm formation and dispersal are considered central to disease transmission. While biofilm formation is well-studied, almost nothing is known about biofilm dispersal. Here, we conduct an imaging screen for V. cholerae mutants that fail to disperse, revealing three classes of dispersal components: signal transduction proteins, matrix-degradation enzymes, and motility factors. Signaling proteins dominated the screen and among them, we focused on an uncharacterized two-component sensory system that we name DbfS/DbfR for Dispersal of Biofilm Sensor/Regulator. Phospho-DbfR represses biofilm dispersal. DbfS dephosphorylates and thereby inactivates DbfR, which permits dispersal. Matrix degradation requires two enzymes: LapG, which cleaves adhesins, and RbmB, which digests matrix polysaccharide. Reorientations in swimming direction, mediated by CheY3, are necessary for cells to escape from the porous biofilm matrix. We suggest that these components act sequentially: signaling launches dispersal by terminating matrix production and triggering matrix digestion and, subsequently, cell motility permits escape from biofilms. This study lays the groundwork for interventions that modulate V. cholerae biofilm dispersal to ameliorate disease.Significance statementThe pathogen Vibrio cholerae alternates between the free-swimming state and existing in sessile multicellular communities known as biofilms. Transitioning between these lifestyles is key for disease transmission. V. cholerae biofilm formation is well studied, however, almost nothing is known about how V. cholerae cells disperse from biofilms, precluding understanding of a central pathogenicity step. Here, we conducted a high-content imaging screen for V. cholerae mutants that failed to disperse. Our screen revealed three classes of components required for dispersal: signal transduction, matrix degradation, and motility factors. We characterized these components to reveal the sequence of molecular events that choreograph V. cholerae biofilm dispersal. Our report provides a framework for developing strategies to modulate biofilm dispersal to prevent or treat disease.

scholarly journals Toxin-Antitoxin Systems in Escherichia coli Influence Biofilm Formation through YjgK (TabA) and Fimbriae

2008 ◽  
Vol 191 (4) ◽  
pp. 1258-1267 ◽  
Author(s):  
Younghoon Kim ◽  
Xiaoxue Wang ◽  
Qun Ma ◽  
Xue-Song Zhang ◽  
Thomas K. Wood
Keyword(s):  
Biofilm Formation ◽  
Cell Attachment ◽  
Single Gene ◽  
Transcriptome Profiling ◽  
Uncharacterized Protein ◽  
Qrt Pcr ◽  
Biofilm Dispersal ◽  
Biofilm Development ◽  
Whole Transcriptome

ABSTRACT The roles of toxin-antitoxin (TA) systems in bacteria have been debated. Here, the role of five TA systems in regard to biofilm development was investigated (listed as toxin/antitoxin: MazF/MazE, RelE/RelB, ChpB, YoeB/YefM, and YafQ/DinJ). Although these multiple TA systems were reported previously to not impact bacterial fitness, we found that deletion of the five TA systems decreased biofilm formation initially (8 h) on three different surfaces and then increased biofilm formation (24 h) by decreasing biofilm dispersal. Whole-transcriptome profiling revealed that the deletion of the five TA systems induced expression of a single gene, yjgK, which encodes an uncharacterized protein; quantitative real-time PCR (qRT-PCR) confirmed consistent induction of this gene (at 8, 15, and 24 h). Corroborating the complex phenotype seen upon deleting the TA systems, overexpression of YjgK decreased biofilm formation at 8 h and increased biofilm formation at 24 h; deletion of yjgK also affected biofilm formation in the expected manner by increasing biofilm formation after 8 h and decreasing biofilm formation after 24 h. In addition, YjgK significantly reduced biofilm dispersal. Whole-transcriptome profiling revealed YjgK represses fimbria genes at 8 h (corroborated by qRT-PCR and a yeast agglutination assay), which agrees with the decrease in biofilm formation upon deleting the five TA systems at 8 h, as well as that seen upon overexpressing YjgK. Sand column assays confirmed that deleting the five TA systems reduced cell attachment. Furthermore, deletion of each of the five toxins increased biofilm formation at 8 h, and overexpression of the five toxins repressed biofilm formation at 8 h, a result that is opposite that of deleting all five TA systems; this suggests that complex regulation occurs involving the antitoxins. Also, the ability of the global regulator Hha to reduce biofilm formation was dependent on the presence of these TA systems. Hence, we suggest that one role of TA systems is to influence biofilm formation.

scholarly journals Identification and Characterization of OscR, a Transcriptional Regulator Involved in Osmolarity Adaptation in Vibrio cholerae

2009 ◽  
Vol 191 (13) ◽  
pp. 4082-4096 ◽  
Author(s):  
Nicholas J. Shikuma ◽  
Fitnat H. Yildiz
Keyword(s):  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Transcriptional Regulator ◽  
Dependent Manner ◽  
Genome Wide ◽  
Low Salt ◽  
Adaptation Response ◽  
Matrix Production ◽  
Identification And Characterization

ABSTRACT Vibrio cholerae is a facultative human pathogen. In its aquatic habitat and as it passes through the digestive tract, V. cholerae must cope with fluctuations in salinity. We analyzed the genome-wide transcriptional profile of V. cholerae grown at different NaCl concentrations and determined that the expression of compatible solute biosynthesis and transporter genes, virulence genes, and genes involved in adhesion and biofilm formation is differentially regulated. We determined that salinity modulates biofilm formation, and this response was mediated through the transcriptional regulators VpsR and VpsT. Additionally, a transcriptional regulator controlling an osmolarity adaptation response was identified. This regulator, OscR (osmolarity controlled regulator), was found to modulate the transcription of genes involved in biofilm matrix production and motility in a salinity-dependent manner. oscR mutants were less motile and exhibited enhanced biofilm formation only under low-salt conditions.

scholarly journals Periodicity of Cell Attachment Patterns during Escherichia coli Biofilm Development

2003 ◽  
Vol 185 (18) ◽  
pp. 5632-5638 ◽  
Author(s):  
Konstantin Agladze ◽  
Debra Jackson ◽  
Tony Romeo
Keyword(s):  
Escherichia Coli ◽  
Laminar Flow ◽  
Biofilm Formation ◽  
Cell Attachment ◽  
Bacterial Biofilms ◽  
Flow Conditions ◽  
Biofilm Development ◽  
Complex Architecture ◽  
Activator Inhibitor ◽  
Laminar Flow Conditions

ABSTRACT The complex architecture of bacterial biofilms inevitably raises the question of their design. Microstructure of developing Escherichia coli biofilms was analyzed under static and laminar flow conditions. Cell attachment during early biofilm formation exhibited periodic density patterns that persisted during development. Several models for the origination of biofilm microstructure are considered, including an activator-inhibitor or Turing model.

scholarly journals Selective Accumulation of Raft-Associated Membrane Protein Lat in T Cell Receptor Signaling Assemblies

2000 ◽  
Vol 151 (2) ◽  
pp. 199-208 ◽  
Author(s):  
Thomas Harder ◽  
Marina Kuhn
Keyword(s):  
Signal Transduction ◽  
Plasma Membrane ◽  
T Cell ◽  
Membrane Protein ◽  
Transmembrane Protein ◽  
Leukemic Cells ◽  
Signaling Proteins ◽  
Dependent Manner ◽  
Tcr Signal Transduction ◽  
Signal Transduction Proteins

Activation of T cell antigen receptor (TCR) induces tyrosine phosphorylations that mediate the assembly of signaling protein complexes. Moreover, cholesterol-sphingolipid raft membrane domains have been implicated to play a role in TCR signal transduction. Here, we studied the assembly of TCR with signal transduction proteins and raft markers in plasma membrane subdomains of Jurkat T leukemic cells. We employed a novel method to immunoisolate plasma membrane subfragments that were highly concentrated in activated TCR–CD3 complexes and associated signaling proteins. We found that the raft transmembrane protein linker for activation of T cells (LAT), but not a palmitoylation-deficient non-raft LAT mutant, strongly accumulated in TCR-enriched immunoisolates in a tyrosine phosphorylation–dependent manner. In contrast, other raft-associated molecules, including protein tyrosine kinases Lck and Fyn, GM1, and cholesterol, were not highly concentrated in TCR-enriched plasma membrane immunoisolates. Many downstream signaling proteins coisolated with the TCR/LAT-enriched plasma membrane fragments, suggesting that LAT/TCR assemblies form a structural scaffold for TCR signal transduction proteins. Our results indicate that TCR signaling assemblies in plasma membrane subdomains, rather than generally concentrating raft-associated membrane proteins and lipids, form by a selective protein-mediated anchoring of the raft membrane protein LAT in vicinity of TCR.

Interspecies Interactions of Metal-Oxidizing Thermo-Acidophilic Archaea Acidianus and Sulfolobus

2015 ◽  
Vol 1130 ◽  
pp. 105-108 ◽  
Author(s):  
Rui Yong Zhang ◽  
Jing Liu ◽  
Thomas R. Neu ◽  
Qian Li ◽  
Sören Bellenberg ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Laser Scanning ◽  
Fluorescent Dyes ◽  
Mine Drainage ◽  
Cell Attachment ◽  
Thermophilic Bacteria ◽  
Laser Scanning Microscopy ◽  
Physical Contact ◽  
Confocal Laser ◽  
Acidophilic Archaea

Biofilm formation of microorganisms on relevant surfaces is of great importance for biomining and acid mine drainage (AMD). Thermo-acidophilic archaea like Acidianus, Sulfolobus and Metallosphaera are of special interest due to their ability to enhance leaching rates. Visualization and investigation of microbial attachment and biofilm formation of metal-oxidizing organisms up to now has been done mostly with mesophilic or moderately thermophilic bacteria. In this study, attachment and biofilms by the crenarchaeota Sulfolobus metallicus DSM 6482T and a new isolate Acidianus sp. DSM 29099 on sulfur or pyrite were analyzed. Confocal laser scanning microscopy (CLSM) combined with fluorescent dyes specific for nucleic acids or glycoconjugates were used to monitor biofilm formation on surfaces. The data indicate that cell attachment and the subsequently formed biofilm structures were species and substrate dependent. The investigation of binary biofilms on pyrite showed that both species were heterogeneously distributed on pyrite surfaces in the form of individual cells or microcolonies. In addition, physical contact between the two species was visible, as revealed by specific lectins able to distinguish single species.

scholarly journals Chicken Juice Enhances Surface Attachment and Biofilm Formation of Campylobacter jejuni

2014 ◽  
Vol 80 (22) ◽  
pp. 7053-7060 ◽  
Author(s):  
Helen L. Brown ◽  
Mark Reuter ◽  
Louise J. Salt ◽  
Kathryn L. Cross ◽  
Roy P. Betts ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Food Chain ◽  
Biofilm Formation ◽  
Cell Attachment ◽  
Bacterial Attachment ◽  
Poultry Meat ◽  
Abiotic Surface ◽  
Surface Attachment ◽  
Aerobic Conditions ◽  
Content Type

ABSTRACTThe bacterial pathogenCampylobacter jejuniis primarily transmitted via the consumption of contaminated foodstuffs, especially poultry meat. In food processing environments,C. jejuniis required to survive a multitude of stresses and requires the use of specific survival mechanisms, such as biofilms. An initial step in biofilm formation is bacterial attachment to a surface. Here, we investigated the effects of a chicken meat exudate (chicken juice) onC. jejunisurface attachment and biofilm formation. Supplementation of brucella broth with ≥5% chicken juice resulted in increased biofilm formation on glass, polystyrene, and stainless steel surfaces with fourC. jejuniisolates and oneC. coliisolate in both microaerobic and aerobic conditions. When incubated with chicken juice,C. jejuniwas both able to grow and form biofilms in static cultures in aerobic conditions. Electron microscopy showed thatC. jejunicells were associated with chicken juice particulates attached to the abiotic surface rather than the surface itself. This suggests that chicken juice contributes toC. jejunibiofilm formation by covering and conditioning the abiotic surface and is a source of nutrients. Chicken juice was able to complement the reduction in biofilm formation of an aflagellated mutant ofC. jejuni, indicating that chicken juice may support food chain transmission of isolates with lowered motility. We provide here a useful model for studying the interaction ofC. jejunibiofilms in food chain-relevant conditions and also show a possible mechanism forC. jejunicell attachment and biofilm initiation on abiotic surfaces within the food chain.

scholarly journals Signals, Regulatory Networks, and Materials That Build and Break Bacterial Biofilms

2009 ◽  
Vol 73 (2) ◽  
pp. 310-347 ◽  
Author(s):  
Ece Karatan ◽  
Paula Watnick
Keyword(s):  
Signaling Pathways ◽  
Biofilm Formation ◽  
Regulatory Networks ◽  
Bacterial Species ◽  
Large Body ◽  
Current Understanding ◽  
Bacterial Biofilms ◽  
Environmental Signals ◽  
Biofilm Dispersal ◽  
Biofilm Matrix

SUMMARY Biofilms are communities of microorganisms that live attached to surfaces. Biofilm formation has received much attention in the last decade, as it has become clear that virtually all types of bacteria can form biofilms and that this may be the preferred mode of bacterial existence in nature. Our current understanding of biofilm formation is based on numerous studies of myriad bacterial species. Here, we review a portion of this large body of work including the environmental signals and signaling pathways that regulate biofilm formation, the components of the biofilm matrix, and the mechanisms and regulation of biofilm dispersal.

scholarly journals Induction of native c-di-GMP phosphodiesterases leads to dispersal of Pseudomonas aeruginosa biofilms

2021 ◽  
Author(s):  
Jens Bo Andersen ◽  
Kasper Nørskov Kragh ◽  
Louise Dahl Hultqvist ◽  
Morten Rybtke ◽  
Martin Nilsson ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Pseudomonas Aeruginosa ◽  
Single Cell ◽  
Biofilm Formation ◽  
Ectopic Expression ◽  
Second Messenger ◽  
Flow Cell ◽  
Diguanylate Cyclases ◽  
Biofilm Dispersal ◽  
High Level

A decade of research has shown that the molecule c-di-GMP functions as a central second messenger in many bacteria. A high level of c-di-GMP is associated with biofilm formation whereas a low level of c-di-GMP is associated with a planktonic single-cell bacterial lifestyle. C-di-GMP is formed by diguanylate cyclases and is degraded by specific phosphodiesterases. We have previously presented evidence that ectopic expression in Pseudomonas aeruginosa of the Escherichia coli phosphodiesterase YhjH results in biofilm dispersal. More recently, however, evidence has been presented that induction of native c-di-GMP phosphodiesterases does not lead to dispersal of P. aeruginosa biofilms. The latter result may discourage attempts to use c-di-GMP signaling as a target for development of anti-biofilm drugs. However, here we demonstrate that induction of the P. aeruginosa c-di-GMP phosphodiesterases PA2133 and BifA indeed does result in dispersal of P. aeruginosa biofilms in both a microtiter tray biofilm assay and in a flow-cell biofilm system.

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