scholarly journals Quorum Sensing of Acidophiles: A Communication System in Microorganisms

2021 ◽  
Author(s):  
Xueyan Gao ◽  
Jianqiang Lin ◽  
Linxu Chen ◽  
Jianqun Lin ◽  
Xin Pang

Communication is important for organisms living in nature. Quorum sensing system (QS) are intercellular communication systems that promote the sociality of microbes. Microorganisms could promote cell-to-cell cooperation and population density to adapt to the changing environment through QS-mediated regulation that is dependent on the secretion and the detection of signal molecules (or called autoinducers). QS system is also discovered in acidophiles, a microorganism that is widely used in the bioleaching industry and can live in an acidic environment. An example is the LuxI/R-like QS system (AfeI/R) that has been reported in the chemoautotrophic species of the genus Acidithiobacillus. In this chapter, we will introduce the types and distribution of the QS system, and the biological function and regulatory mechanism of QS in acidophiles. We will also discuss the potential ecological function of QS system and the application value of the QS system in the control and regulation of the bioleaching process in the related industries and acid mine damage.

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Iztok Dogsa ◽  
Mihael Spacapan ◽  
Anna Dragoš ◽  
Tjaša Danevčič ◽  
Žiga Pandur ◽  
...  

AbstractBacterial quorum sensing (QS) is based on signal molecules (SM), which increase in concentration with cell density. At critical SM concentration, a variety of adaptive genes sharply change their expression from basic level to maximum level. In general, this sharp transition, a hallmark of true QS, requires an SM dependent positive feedback loop, where SM enhances its own production. Some communication systems, like the peptide SM-based ComQXPA communication system of Bacillus subtilis, do not have this feedback loop and we do not understand how and if the sharp transition in gene expression is achieved. Based on experiments and mathematical modeling, we observed that the SM peptide ComX encodes the information about cell density, specific cell growth rate, and even oxygen concentration, which ensure power-law increase in SM production. This enables together with the cooperative response to SM (ComX) a sharp transition in gene expression level and this without the SM dependent feedback loop. Due to its ultra-sensitive nature, the ComQXPA can operate at SM concentrations that are 100–1000 times lower than typically found in other QS systems, thereby substantially reducing the total metabolic cost of otherwise expensive ComX peptide.


Lab on a Chip ◽  
2015 ◽  
Vol 15 (3) ◽  
pp. 889-899 ◽  
Author(s):  
Heon-Ho Jeong ◽  
Si Hyung Jin ◽  
Byung Jin Lee ◽  
Taesung Kim ◽  
Chang-Soo Lee

Quorum sensing (QS) is a type of cell–cell communication using signal molecules that are released and detected by cells, which respond to changes in their population density.


2004 ◽  
Vol 186 (20) ◽  
pp. 6902-6914 ◽  
Author(s):  
Jennifer M. Henke ◽  
Bonnie L. Bassler

ABSTRACT In a process called quorum sensing, bacteria communicate using extracellular signal molecules termed autoinducers. Two parallel quorum-sensing systems have been identified in the marine bacterium Vibrio harveyi. System 1 consists of the LuxM-dependent autoinducer HAI-1 and the HAI-1 sensor, LuxN. System 2 consists of the LuxS-dependent autoinducer AI-2 and the AI-2 detector, LuxPQ. The related bacterium, Vibrio cholerae, a human pathogen, possesses System 2 (LuxS, AI-2, and LuxPQ) but does not have obvious homologues of V. harveyi System 1. Rather, System 1 of V. cholerae is made up of the CqsA-dependent autoinducer CAI-1 and a sensor called CqsS. Using a V. cholerae CAI-1 reporter strain we show that many other marine bacteria, including V. harveyi, produce CAI-1 activity. Genetic analysis of V. harveyi reveals cqsA and cqsS, and phenotypic analysis of V. harveyi cqsA and cqsS mutants shows that these functions comprise a third V. harveyi quorum-sensing system that acts in parallel to Systems 1 and 2. Together these communication systems act as a three-way coincidence detector in the regulation of a variety of genes, including those responsible for bioluminescence, type III secretion, and metalloprotease production.


2000 ◽  
Vol 355 (1397) ◽  
pp. 667-680 ◽  
Author(s):  
Paul Williams ◽  
Miguel Camara ◽  
Andrea Hardman ◽  
Simon Swift ◽  
Deborah Milton ◽  
...  

One crucial feature of almost all bacterial infections is the need for the invading pathogen to reach a critical cell population density sufficient to overcome host defences and establish the infection. Controlling the expression of virulence determinants in concert with cell population density may therefore confer a significant survival advantage on the pathogen such that the host is overwhelmed before a defence response can be fully initiated. Many different bacterial pathogens are now known to regulate diverse physiological processes including virulence in a cell–density–dependent manner through cell–cell communication. This phenomenon, which relies on the interaction of a diffusible signal molecule (e.g. an N –acylhomoserine lactone) with a sensor or transcriptional activator to couple gene expression with cell population density, has become known as ‘quorum sensing’ . Although the size of the ‘quorum’ is likely to be highly variable and influenced by the diffusibility of the signal molecule within infected tissues, nevertheless quorum–sensing signal molecules can be detected in vivo in both experimental animal model and human infections. Furthermore, certain quorum–sensing molecules have been shown to possess pharmacological and immunomodulatory activity such that they may function as virulence determinants per se . As a consequence, quorum sensing constitutes a novel therapeutic target for the design of small molecular antagonists capable of attenuating virulence through the blockade of bacterial cell–cell communication.


Microbiology ◽  
2003 ◽  
Vol 149 (7) ◽  
pp. 1923-1933 ◽  
Author(s):  
Diane McDougald ◽  
Sujatha Srinivasan ◽  
Scott A. Rice ◽  
Staffan Kjelleberg

Quorum sensing systems serve as a means of ‘census taking’ of conspecific and non-conspecific bacteria in the near vicinity. The acylated homoserine lactone (AHL) quorum sensing system has been proposed to be primarily an intra-specific communication system, while the AI-2 autoinducer signalling system is proposed to be an interspecific communication system. Here it is shown that AI-2-like signalling in two marine Vibrio species, Vibrio vulnificus and ‘Vibrio angustum’ S14, induces the core response phenotypes of starvation adaptation and stress resistance, and that a signal antagonist can competitively inhibit these phenotypes. Furthermore, the signals produced by a range of Vibrio species have the ability to induce these phenotypes in V. vulnificus and ‘V. angustum’ S14, indicating that, at least in Vibrio species, AI-2-like signalling systems function as interspecies communication systems capable of ‘cross-talk’ and of regulating environmentally relevant phenotypes.


2020 ◽  
Author(s):  
Kate Rahbari ◽  
Jennifer Chang ◽  
Michael Federle

AbstractSome bacterial pathogens utilize cell-cell communication systems, such as quorum sensing (QS), to coordinate genetic programs during host colonization and infection. The human-restricted pathosymbiont Streptococcus pyogenes (Group A Streptococcus, GAS) uses the Rgg2/Rgg3 QS system to modify the bacterial surface, enabling biofilm formation and lysozyme resistance. Here, we demonstrate that innate immune cell responses to GAS are substantially altered by the QS status of the bacteria. We found that macrophage activation, stimulated by multiple agonists and assessed by cytokine production and NFκB activity, was substantially suppressed upon interaction with QS-active GAS but not QS-inactive bacteria. Neither macrophage viability nor bacterial adherence were seen as different between QS activity states, yet TNFα, IL-6, and IFNβ levels and NFκB reporter activity were drastically lower following infection with QS-active GAS. Suppression required contact between viable bacteria and macrophages. A QS-regulated biosynthetic gene cluster (BGC) in the GAS genome, encoding several putative enzymes, was also required for macrophage modulation. Our findings suggest a model wherein upon contact with macrophages, QS-active GAS produce a BGC-derived factor capable of suppressing inflammatory responses. The suppressive capability of QS-active GAS is abolished after treatment with a specific QS inhibitor. These observations suggest that interfering with the ability of bacteria to collaborate via QS can serve as a strategy to counteract microbial efforts to manipulate host defenses.ImportanceStreptococcus pyogenes is restricted to human hosts and commonly causes superficial diseases such as pharyngitis; it can also cause severe and deadly manifestations including necrotizing skin disease or severe post-infectious sequelae like rheumatic heart disease. Understanding the complex mechanisms used by this pathogen to manipulate host defenses could aid in developing new therapeutics to treat infections. Here, we examine the impact of a bacterial cell-cell communication system, which is highly conserved across S. pyogenes, on host innate immune responses. We find that S. pyogenes uses this system to suppress macrophage pro-inflammatory cytokine responses. Interference with this communication system could serve as a strategy to disarm bacteria and maintain an effective immune response.


mBio ◽  
2021 ◽  
Vol 12 (3) ◽  
Author(s):  
Kate M. Rahbari ◽  
Jennifer C. Chang ◽  
Michael J. Federle

ABSTRACT Some bacterial pathogens utilize cell-cell communication systems, such as quorum sensing (QS), to coordinate genetic programs during host colonization and infection. The human-restricted pathosymbiont Streptococcus pyogenes (group A streptococcus [GAS]) uses the Rgg2/Rgg3 QS system to modify the bacterial surface, enabling biofilm formation and lysozyme resistance. Here, we demonstrate that innate immune cell responses to GAS are substantially altered by the QS status of the bacteria. We found that macrophage activation, stimulated by multiple agonists and assessed by cytokine production and NF-κB activity, was substantially suppressed upon interaction with QS-active GAS but not QS-inactive bacteria. Neither macrophage viability nor bacterial adherence, internalization, or survival were altered by the QS activation status, yet tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and interferon beta (IFN-β) levels and NF-κB reporter activity were drastically lower following infection with QS-active GAS. Suppression required contact between viable bacteria and macrophages. A QS-regulated biosynthetic gene cluster (BGC) in the GAS genome, encoding several putative enzymes, was also required for macrophage modulation. Our findings suggest a model wherein upon contact with macrophages, QS-active GAS produce a BGC-derived factor capable of suppressing inflammatory responses. The suppressive capability of QS-active GAS is abolished after treatment with a specific QS inhibitor. These observations suggest that interfering with the ability of bacteria to collaborate via QS can serve as a strategy to counteract microbial efforts to manipulate host defenses. IMPORTANCE Streptococcus pyogenes is restricted to human hosts and commonly causes superficial diseases such as pharyngitis; it can also cause severe and deadly manifestations including necrotizing skin disease or severe postinfectious sequelae like rheumatic heart disease. Understanding the complex mechanisms used by this pathogen to manipulate host defenses could aid in developing new therapeutics to treat infections. Here, we examine the impact of a bacterial cell-cell communication system, which is highly conserved across S. pyogenes, on host innate immune responses. We find that S. pyogenes uses this system to suppress macrophage proinflammatory cytokine responses in vitro. Interference with this communication system could serve as a strategy to disarm bacteria and maintain an effective immune response.


2020 ◽  
Vol 17 (4) ◽  
pp. 498-506 ◽  
Author(s):  
Pavan K. Mujawdiya ◽  
Suman Kapur

: Quorum Sensing (QS) is a phenomenon in which bacterial cells communicate with each other with the help of several low molecular weight compounds. QS is largely dependent on population density, and it triggers when the concentration of quorum sensing molecules accumulate in the environment and crosses a particular threshold. Once a certain population density is achieved and the concentration of molecules crosses a threshold, the bacterial cells show a collective behavior in response to various chemical stimuli referred to as “auto-inducers”. The QS signaling is crucial for several phenotypic characteristics responsible for bacterial survival such as motility, virulence, and biofilm formation. Biofilm formation is also responsible for making bacterial cells resistant to antibiotics. : The human gut is home to trillions of bacterial cells collectively called “gut microbiota” or “gut microbes”. Gut microbes are a consortium of more than 15,000 bacterial species and play a very crucial role in several body functions such as metabolism, development and maturation of the immune system, and the synthesis of several essential vitamins. Due to its critical role in shaping human survival and its modulating impact on body metabolisms, the gut microbial community has been referred to as “the forgotten organ” by O`Hara et al. (2006) [1]. Several studies have demonstrated that chemical interaction between the members of bacterial cells in the gut is responsible for shaping the overall microbial community. : Recent advances in phytochemical research have generated a lot of interest in finding new, effective, and safer alternatives to modern chemical-based medicines. In the context of antimicrobial research various plant extracts have been identified with Quorum Sensing Inhibitory (QSI) activities among bacterial cells. This review focuses on the mechanism of quorum sensing and quorum sensing inhibitors isolated from natural sources.


Author(s):  
Kamal Hamid ◽  
Nadim Chahine

Wireless communications became one of the most widespread means for transferring information. Speed and reliability in transferring the piece of information are considered one of the most important requirements in communication systems in general. Moreover, Quality and reliability in any system are considered the most important criterion of the efficiency of this system in doing the task it is designed to do and its ability for satisfactory performance for a certain period of time, Therefore, we need fault tree analysis in these systems in order to determine how to detect an error or defect when happening in communication system and what are the possibilities that make this error happens. This research deals with studying TETRA system components, studying the physical layer in theory and practice, as well as studying fault tree analysis in this system, and later benefit from this study in proposing improvements to the structure of the system, which led to improve gain in Link Budget. A simulation and test have been done using MATLAB, where simulation results have shown that the built fault tree is able to detect the system’s work by 82.4%.


2020 ◽  
Vol 74 (1) ◽  
pp. 587-606 ◽  
Author(s):  
Nitzan Aframian ◽  
Avigdor Eldar

Quorum sensing is a process in which bacteria secrete and sense a diffusible molecule, thereby enabling bacterial groups to coordinate their behavior in a density-dependent manner. Quorum sensing has evolved multiple times independently, utilizing different molecular pathways and signaling molecules. A common theme among many quorum-sensing families is their wide range of signaling diversity—different variants within a family code for different signal molecules with a cognate receptor specific to each variant. This pattern of vast allelic polymorphism raises several questions—How do different signaling variants interact with one another? How is this diversity maintained? And how did it come to exist in the first place? Here we argue that social interactions between signaling variants can explain the emergence and persistence of signaling diversity throughout evolution. Finally, we extend the discussion to include cases where multiple diverse systems work in concert in a single bacterium.


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