From Input to Output: The Lap/c-di-GMP Biofilm Regulatory Circuit

2020 ◽  
Vol 74 (1) ◽  
pp. 607-631 ◽  
Author(s):  
Alan J. Collins ◽  
T. Jarrod Smith ◽  
Holger Sondermann ◽  
George A. O'Toole
Keyword(s):  
Biofilm Formation ◽  
Secretion System ◽  
Bacterial Biofilm ◽  
Classical Type ◽  
Bacterial Biofilms ◽  
Type I ◽  
Metabolizing Enzymes ◽  
Regulatory Circuit ◽  
The Subject ◽  
And Function

Biofilms are the dominant bacterial lifestyle. The regulation of the formation and dispersal of bacterial biofilms has been the subject of study in many organisms. Over the last two decades, the mechanisms of Pseudomonas fluorescens biofilm formation and regulation have emerged as among the best understood of any bacterial biofilm system. Biofilm formation by P. fluorescens occurs through the localization of an adhesin, LapA, to the outer membrane via a variant of the classical type I secretion system. The decision between biofilm formation and dispersal is mediated by LapD, a c-di-GMP receptor, and LapG, a periplasmic protease, which together control whether LapA is retained or released from the cell surface. LapA localization is also controlled by a complex network of c-di-GMP-metabolizing enzymes. This review describes the current understanding of LapA-mediated biofilm formation by P. fluorescens and discusses several emerging models for the regulation and function of this adhesin.

scholarly journals A Conserved Regulatory Circuit Controls Large Adhesins in Vibrio cholerae

mBio ◽  
2019 ◽  
Vol 10 (6) ◽  
Author(s):  
Giordan Kitts ◽  
Krista M. Giglio ◽  
David Zamorano-Sánchez ◽  
Jin Hwan Park ◽  
Loni Townsley ◽  
...  
Keyword(s):  
Cell Surface ◽  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Diarrheal Disease ◽  
Cell Attachment ◽  
Surface Display ◽  
Second Messenger ◽  
Bacterial Biofilm ◽  
Content Type ◽  
Regulatory Circuit

ABSTRACT The dinucleotide second messenger c-di-GMP has emerged as a central regulator of reversible cell attachment during bacterial biofilm formation. A prominent cell adhesion mechanism first identified in pseudomonads combines two c-di-GMP-mediated processes: transcription of a large adhesin and its cell surface display via posttranslational proteolytic control. Here, we characterize an orthologous c-di-GMP effector system and show that it is operational in Vibrio cholerae, where it regulates two distinct classes of adhesins. Through structural analyses, we reveal a conserved autoinhibition mechanism of the c-di-GMP receptor that controls adhesin proteolysis and present a structure of a c-di-GMP-bound receptor module. We further establish functionality of the periplasmic protease controlled by the receptor against the two adhesins. Finally, transcription and functional assays identify physiological roles of both c-di-GMP-regulated adhesins in surface attachment and biofilm formation. Together, our studies highlight the conservation of a highly efficient signaling effector circuit for the control of cell surface adhesin expression and its versatility by revealing strain-specific variations. IMPORTANCE Vibrio cholerae, the causative agent of the diarrheal disease cholera, benefits from a sessile biofilm lifestyle that enhances survival outside the host but also contributes to host colonization and infectivity. The bacterial second messenger c-di-GMP has been identified as a central regulator of biofilm formation, including in V. cholerae; however, our understanding of the pathways that contribute to this process is incomplete. Here, we define a conserved signaling system that controls the stability of large adhesion proteins at the cell surface of V. cholerae, which are important for cell attachment and biofilm formation. Insight into the regulatory circuit underlying biofilm formation may inform targeted strategies to interfere with a process that renders this bacterium remarkably adaptable to changing environments.

scholarly journals Bacterial Biofilm Formation Using PCL/Curcumin Electrospun Fibers and Its Potential Use for Biotechnological Applications

Materials ◽  
2020 ◽  
Vol 13 (23) ◽  
pp. 5556
Author(s):  
Daniella Alejandra Pompa-Monroy ◽  
Paulina Guadalupe Figueroa-Marchant ◽  
Syed G. Dastager ◽  
Meghana Namdeo Thorat ◽  
Ana Leticia Iglesias ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Food Industry ◽  
Electrospun Nanofibers ◽  
Bacterial Biofilm ◽  
Bacterial Biofilms ◽  
Scanning Calorimetry ◽  
Metabolites Production ◽  
Pathogenic Biofilms ◽  
Tga And Dsc ◽  
Potential Use

Electrospun nanofibers are used for many applications due to their large surface area, mechanical properties, and bioactivity. Bacterial biofilms are the cause of numerous problems in biomedical devices and in the food industry. On the other hand, these bacterial biofilms can produce interesting metabolites. Hence, the objective of this study is to evaluate the efficiency of poly (Ɛ- caprolactone)/Curcumin (PCL/CUR) nanofibers to promote bacterial biofilm formation. These scaffolds were characterized by scanning electron microscopy (SEM), which showed homogeneous fibers with diameters between 441–557 nm; thermogravimetric analysis and differential scanning calorimetry (TGA and DSC) demonstrated high temperature resilience with degradation temperatures over >350 °C; FTIR and 1H-NMR serve as evidence of CUR incorporation in the PCL fibers. PCL/CUR scaffolds successfully promoted the formation of Escherichia coli, Staphylococcus aureus and Pseudomonas aeruginosa biofilms. These results will be valuable in the study of controlled harvesting of pathogenic biofilms as well as in metabolites production for biotechnological purposes.

scholarly journals Inactivation of Efflux Pumps Abolishes Bacterial Biofilm Formation

2008 ◽  
Vol 74 (23) ◽  
pp. 7376-7382 ◽  
Author(s):  
Malin Kvist ◽  
Viktoria Hancock ◽  
Per Klemm
Keyword(s):  
Health Care ◽  
Biofilm Formation ◽  
Efflux Pump ◽  
Efflux Pumps ◽  
Bacterial Biofilm ◽  
Bacterial Biofilms ◽  
Toxic Substances ◽  
Highly Active ◽  
Efflux Pump Inhibitors ◽  
New Treatments

ABSTRACT Bacterial biofilms cause numerous problems in health care and industry; notably, biofilms are associated with a large number of infections. Biofilm-dwelling bacteria are particularly resistant to antibiotics, making it hard to eradicate biofilm-associated infections. Bacteria rely on efflux pumps to get rid of toxic substances. We discovered that efflux pumps are highly active in bacterial biofilms, thus making efflux pumps attractive targets for antibiofilm measures. A number of efflux pump inhibitors (EPIs) are known. EPIs were shown to reduce biofilm formation, and in combination they could abolish biofilm formation completely. Also, EPIs were able to block the antibiotic tolerance of biofilms. The results of this feasibility study might pave the way for new treatments for biofilm-related infections and may be exploited for prevention of biofilms in general.

scholarly journals A Novel Autoantibody Induced by Bacterial Biofilm Conserved Components Aggravates Lupus Nephritis

2021 ◽  
Vol 12 ◽  
Author(s):  
Wenyan Fu ◽  
Yu Liu ◽  
Fangjie Liu ◽  
Chenghua Liu ◽  
Jingjing Li ◽  
...  
Keyword(s):  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Biofilm Formation ◽  
Protein Disulfide Isomerase ◽  
Bacterial Biofilm ◽  
Systemic Autoimmune Disease ◽  
Bacterial Biofilms ◽  
Autoantibody Production ◽  
Disulfide Isomerase ◽  
Protein Disulfide

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with multiple autoantibody production and often affects the kidneys, known as lupus nephritis. However, the mechanism underlying lupus nephritis development is unclear. Biofilms that protect bacteria from stress are ubiquitous in almost every environment. Here, we identified that a conserved peptide (HU1) derived from DNABII proteins, one of major bacterial biofilm components, was specifically recognized by sera from about 47% patients with SLE. Moreover, the serum anti-HU1 levels showed a significant positive correlation with lupus nephritis occurrence. Presence of antibodies against HU1 in pristane-induced mice aggravated lupus nephritis, although these antibodies also attenuated bacterial biofilm formation. We further identified that antibodies against HU1 cross-recognized protein disulfide isomerase (P4HB) located on the renal cell surface and inhibited the activities of this enzyme. Our findings reveal a novel mechanism underlying the development of lupus nephritis triggered by bacterial biofilms.

A family of transmembrane microneme proteins ofToxoplasma gondiicontain EGF-like domains and function as escorters

2002 ◽  
Vol 115 (3) ◽  
pp. 563-574 ◽  
Author(s):  
Markus Meissner ◽  
Matthias Reiss ◽  
Nicola Viebig ◽  
Vern B. Carruthers ◽  
Catherine Toursel ◽  
...  
Keyword(s):  
Secretory Pathway ◽  
Protein Complexes ◽  
Protozoan Parasite ◽  
Membrane Topology ◽  
Classical Type ◽  
Type I ◽  
Sorting Signals ◽  
Epidermal Growth ◽  
And Function ◽  
Golgi Network

TgMIC6, TgMIC7, TgMIC8 and TgMIC9 are members of a novel family of transmembrane proteins localized in the micronemes of the protozoan parasite Toxoplasma gondii. These proteins contain multiple epidermal growth factor-like domains, a putative transmembrane spanning domain and a short cytoplasmic tail. Sorting signals to the micronemes are encoded in this short tail. We established previously that TgMIC6 serves as an escorter for two soluble adhesins, TgMIC1 and TgMIC4. Here, we present the characterization of TgMIC6 and three additional members of this family, TgMIC7, -8 and -9. Consistent with having sorting signals localized in its C-terminal tail,TgMIC6 exhibits a classical type I membrane topology during its transport along the secretory pathway and during storage in the micronemes. TgMIC6 is processed at the N-terminus, probably in the trans-Golgi network, and the cleavage site has been precisely mapped. Additionally, like other members of the thrombospondin-related anonymous protein family, TgMIC2, TgMIC6 and TgMIC8 are proteolytically cleaved near their C-terminal domain upon discharge by micronemes. We also provide evidence that TgMIC8 escorts another recently described soluble adhesin, TgMIC3. This suggests that the existence of microneme protein complexes is not an exception but rather the rule. TgMIC6 and TgMIC8 are expressed in the rapidly dividing tachyzoites, while TgMIC7 and TgMIC9 genes are predominantly expressed in bradyzoites, where they presumably also serve as escorters.

scholarly journals Biofilm formation by Paracoccus denitrificans requires a type I secretion system-dependent adhesin BapA

2017 ◽  
Vol 364 (4) ◽  
Author(s):  
Keitaro Yoshida ◽  
Masanori Toyofuku ◽  
Nozomu Obana ◽  
Nobuhiko Nomura
Keyword(s):  
Biofilm Formation ◽  
Paracoccus Denitrificans ◽  
Secretion System ◽  
Type I

scholarly journals Rhamnolipids and surfactin inhibit the growth or formation of oral bacterial biofilm

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Ryota Yamasaki ◽  
Aki Kawano ◽  
Yoshie Yoshioka ◽  
Wataru Ariyoshi
Keyword(s):  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Oral Bacteria ◽  
Bacterial Biofilm ◽  
Industrial Processes ◽  
Oral Drug ◽  
Bacterial Biofilms ◽  
Effective Inhibition ◽  
Medical Instruments ◽  
Scanning Electron

Abstract Background Bacteria survive in various environments by forming biofilms. Bacterial biofilms often cause significant problems to medical instruments and industrial processes. Techniques to inhibit biofilm formation are essential and have wide applications. In this study, we evaluated the ability of two types of biosurfactants (rhamnolipids and surfactin) to inhibit growth and biofilm formation ability of oral pathogenic bacteria such as Aggregatibacter actinomycetemcomitans, Streptococcus mutans, and Streptococcus sanguinis. Results Rhamnolipids inhibited the growth and biofilm formation ability of all examined oral bacteria. Surfactin showed effective inhibition against S. sanguinis ATCC10556, but lower effects toward A. actinomycetemcomitans Y4 and S. mutans UA159. To corroborate these results, biofilms were observed by scanning electron microscopy (SEM) and confocal microscopy. The observations were largely in concordance with the biofilm assay results. We also attempted to determine the step in the biofilm formation process that was inhibited by biosurfactants. The results clearly demonstrated that rhamnolipids inhibit biofilm formation after the initiation process, however, they do not affect attachment or maturation. Conclusions Rhamnolipids inhibit oral bacterial growth and biofilm formation by A. actinomycetemcomitans Y4, and may serve as novel oral drug against localized invasive periodontitis.

scholarly journals Lucilia sericata Chymotrypsin Disrupts Protein Adhesin-Mediated Staphylococcal Biofilm Formation

2012 ◽  
Vol 79 (4) ◽  
pp. 1393-1395 ◽  
Author(s):  
Llinos G. Harris ◽  
Yamni Nigam ◽  
James Sawyer ◽  
Dietrich Mack ◽  
David I. Pritchard
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Lucilia Sericata ◽  
Bacterial Biofilm ◽  
Bacterial Biofilms ◽  
Formation Mechanisms ◽  
Chronic Infections ◽  
Content Type ◽  
Effective Activity

ABSTRACTStaphylococcus aureusandStaphylococcus epidermidisbiofilms cause chronic infections due to their ability to form biofilms. The excretions/secretions ofLucilia sericatalarvae (maggots) have effective activity for debridement and disruption of bacterial biofilms. In this paper, we demonstrate how chymotrypsin derived from maggot excretions/secretions disrupts protein-dependent bacterial biofilm formation mechanisms.

scholarly journals CRISPR-cas3 of Salmonella Upregulates Bacterial Biofilm Formation and Virulence to Host Cells by Targeting Quorum-Sensing Systems

Pathogens ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 53 ◽  
Author(s):  
Luqing Cui ◽  
Xiangru Wang ◽  
Deyu Huang ◽  
Yue Zhao ◽  
Jiawei Feng ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Biofilm Formation ◽  
Bacterial Biofilm ◽  
Host Cells ◽  
Microbial Pathogens ◽  
Bacterial Invasion ◽  
Type I ◽  
Salmonella Enterica Serovar Enteritidis ◽  
Sensing Systems ◽  
Type Three Secretion System

Salmonella is recognized as one of the most common microbial pathogens worldwide. The bacterium contains the clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR-associated (Cas) systems, providing adaptive immunity against invading foreign nucleic acids. Previous studies suggested that certain bacteria employ the Cas proteins of CRISPR-Cas systems to target their own genes, which also alters the virulence during invasion of mammals. However, whether CRISPR-Cas systems in Salmonella have similar functions during bacterial invasion of host cells remains unknown. Here, we systematically analyzed the genes that are regulated by Cas3 in a type I-E CRISPR-Cas system and the virulence changes due to the deletion of cas3 in Salmonella enterica serovar Enteritidis. Compared to the cas3 gene wild-type (cas3 WT) Salmonella strain, cas3 deletion upregulated the lsrFGBE genes in lsr (luxS regulated) operon related to quorum sensing (QS) and downregulated biofilm-forming-related genes and Salmonella pathogenicity island 1 (SPI-1) genes related to the type three secretion system (T3SS). Consistently, the biofilm formation ability was downregulated in the cas3 deletion mutant (Δcas3). The bacterial invasive and intracellular capacity of Δcas3 to host cells was also reduced, thereby increasing the survival of infected host cells and live chickens. By the transcriptome-wide screen (RNA-Seq), we found that the cas3 gene impacts a series of genes related to QS, the flagellum, and SPI-1-T3SS system, thereby altering the virulence phenotypes. As QS SPI-1-T3SS and CRISPR-Cas systems are widely distributed in the bacteria kingdom, our findings extend our understanding of virulence regulation and pathogenicity in mammalian hosts for Salmonella and potentially other bacteria.

scholarly journals The Pseudomonas aeruginosa Magnesium Transporter MgtE Inhibits Transcription of the Type III Secretion System

2009 ◽  
Vol 78 (3) ◽  
pp. 1239-1249 ◽  
Author(s):  
Gregory G. Anderson ◽  
Timothy L. Yahr ◽  
Rustin R. Lovewell ◽  
George A. O'Toole
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Type Iii Secretion ◽  
Biofilm Formation ◽  
Type Iii Secretion System ◽  
Secretion System ◽  
Bacterial Biofilm ◽  
Magnesium Transport ◽  
Type Iii ◽  
Magnesium Transporter

ABSTRACT Pseudomonas aeruginosa is an opportunistic pathogen that causes life-long pneumonia in individuals with cystic fibrosis (CF). These long-term infections are maintained by bacterial biofilm formation in the CF lung. We have recently developed a model of P. aeruginosa biofilm formation on cultured CF airway epithelial cells. Using this model, we discovered that mutation of a putative magnesium transporter gene, called mgtE, led to increased cytotoxicity of P. aeruginosa toward epithelial cells. This altered toxicity appeared to be dependent upon expression of the type III secretion system (T3SS). In this study, we found that mutation of mgtE results in increased T3SS gene transcription. Through epistasis analyses, we discovered that MgtE influences the ExsE-ExsC-ExsD-ExsA gene regulatory system of T3SS by either directly or indirectly inhibiting ExsA activity. While variations in calcium levels modulate T3SS gene expression in P. aeruginosa, we found that addition of exogenous magnesium did not inhibit T3SS activity. Furthermore, mgtE variants that were defective for magnesium transport could still complement the cytotoxicity effect. Thus, the magnesium transport function of MgtE does not fully explain the regulatory effects of MgtE on cytotoxicity. Overall, our results indicate that MgtE modulates expression of T3SS genes.

Sign in / Sign up

Export Citation Format

Share Document