Quorum-sensing regulators in Gram-positive bacteria: ‘cherchez le peptide ’

2015 ◽  
Vol 97 (2) ◽  
pp. 181-184 ◽  
Author(s):  
V. Monnet ◽  
R. Gardan
2016 ◽  
Vol 39 (8) ◽  
pp. 503-515 ◽  
Author(s):  
Marie Chantal Lemfack ◽  
Srinivasa Rao Ravella ◽  
Nicola Lorenz ◽  
Marco Kai ◽  
Kirsten Jung ◽  
...  

2014 ◽  
pp. 173-192
Author(s):  
S. JABBARI ◽  
J. R. KING ◽  
N. P. MINTON ◽  
K. WINZER

2019 ◽  
Author(s):  
Liqin Zhou ◽  
Leyla Slamti ◽  
Didier Lereclus ◽  
Ben Raymond

AbstractThe persistence of genetic variation in master regulators of gene expression, such as quorum-sensing systems, is hard to explain. Here, we investigated two alternative hypotheses for the prevalence of polymorphic quorum-sensing in Gram-positive bacteria, i.e. the use of different signal / receptor pairs (‘pherotypes’) to regulate the same functions. First, social interactions between pherotypes or ‘facultative cheating’ may favour rare variants that exploit the signals of others. Second, different pherotypes may increase fitness in different environments. We evaluated these hypotheses in the invertebrate pathogen Bacillus thuringiensis, using three pherotypes expressed in a common genetic background. Facultative cheating occurred in homogenized hosts, in contrast, rare pherotypes had reduced fitness in naturalistic infections. There was clear support for environment-dependent fitness: pherotypes varied in responsiveness to signals and in mean competitive fitness. Notably, competitive fitness varied with group size: the pherotype with highest responsiveness to signals performed best in smaller hosts where infections have a lower pathogen group size. Less responsive pherotypes performed best in larger hosts. Results using homogenized insect media fit with the expectation of facultative cheating and social evolution theory, but results from naturalist oral infections do not fit many of the predictions from this body of theory. In this system, low signal abundance appears to limit fitness in hosts while the optimal level of response to signals varies in different host environments.ImportanceQuorum sensing describes the ability of microbes to alter gene regulation according to their local population size. Some successful theory suggests that this is a form of cooperation: investment in shared products is only worthwhile if there are sufficient bacteria making the same product. This theory can explain the genetic diversity in these signaling systems in Gram-positive bacteria such as Bacillus and Staphylococcus. The possible advantages gained by rare genotypes (which can exploit the products of their more common neighbours) could explain why different genotypes can coexist. We show that while these social interactions can occur in simple laboratory experiments they do not occur in naturalistic infections using an invertabrate pathogen, Bacillus thuringiensis. Instead our results suggest that different genotypes are adapted to different-sized hosts. Overall, social models are not easily applied to this system implying that a new explanation for this form of quorum sensing is required.


mBio ◽  
2020 ◽  
Vol 11 (3) ◽  
Author(s):  
Liqin Zhou ◽  
Leyla Slamti ◽  
Didier Lereclus ◽  
Ben Raymond

ABSTRACT The persistence of genetic variation in master regulators of gene expression, such as quorum-sensing systems, is hard to explain. Here, we investigated two alternative hypotheses for the prevalence of polymorphic quorum sensing in Gram-positive bacteria, i.e., the use of different signal/receptor pairs (‘pherotypes’) to regulate the same functions. First, social interactions between pherotypes or ‘facultative cheating’ may favor rare variants that exploit the signals of others. Second, different pherotypes may increase fitness in different environments. We evaluated these hypotheses in the invertebrate pathogen Bacillus thuringiensis, using three pherotypes expressed in a common genetic background. Facultative cheating could occur in well-mixed host homogenates provided there was minimal cross talk between competing pherotypes. However, facultative cheating did not occur when spatial structure was increased in static cultures or in naturalistic oral infections, where common pherotypes had higher fitness. There was clear support for environment-dependent fitness; pherotypes varied in responsiveness to signals and in mean competitive fitness. Notably, competitive fitness varied with group size. In contrast to typical social evolution models of quorum sensing which predict higher response to signal at larger group size, the pherotype with highest responsiveness to signals performed best in smaller hosts where infections have a lower pathogen group size. In this system, low signal abundance appears to limit fitness in hosts, while the optimal level of response to signals varies in different host environments. IMPORTANCE Quorum sensing describes the ability of microbes to alter gene regulation according to their local population size. Some successful theory suggests that this is a form of cooperation, namely, investment in shared products is only worthwhile if there are sufficient bacteria making the same product. This theory can explain the genetic diversity in these signaling systems in Gram-positive bacteria, such as Bacillus and Staphylococcus sp. The possible advantages gained by rare genotypes (which can exploit the products of their more common neighbors) could explain why different genotypes can coexist. We show that while these social interactions can occur in simple laboratory experiments, they do not occur in naturalistic infections using an invertebrate pathogen, Bacillus thuringiensis. Instead, our results suggest that different genotypes are adapted to differently sized hosts. Overall, social models are not easily applied to this system, implying that a different explanation for this form of quorum sensing is required.


2007 ◽  
Vol 30 (9) ◽  
pp. 757-763 ◽  
Author(s):  
J.W. Costerton ◽  
L. Montanaro ◽  
C.r. Arciola

The status of population density is communicated among bacteria by specific secreted molecules, called pheromones or autoinducers, and the control mechanism is called “quorum-sensing”. Quorum-sensing systems regulate the expression of a panel of genes, allowing bacteria to adapt to modified environmental conditions at a high density of population. The two known different quorum systems are described as the LuxR-LuxI system in gram-negative bacteria, which uses an N-acyl-homoserine lactone (AHL) as signal, and the agr system in gram-positive bacteria, which uses a peptide-tiolactone as signal and the RNAIII as effector molecules. Both in gram-negative and in gram-positive bacteria, quorum-sensing systems regulate the expression of adhesion mechanisms (biofilm and adhesins) and virulence factors (toxins and exoenzymes) depending on population cell density. In gram-negative Pseudomonas aeruginosa, analogs of signaling molecules such as furanone analogs, are effective in attenuating bacterial virulence and controlling bacterial infections. In gram-positive Staphylococcus aureus, the quorum-sensing RNAIII-inhibiting peptide (RIP), tested in vitro and in animal infection models, has been proved to inhibit virulence and prevent infections. Attenuation of bacterial virulence by quorum-sensing inhibitors, rather than by bactericidal or bacteriostatic drugs, is a highly attractive concept because these antibacterial agents are less likely to induce the development of bacterial resistance.


2007 ◽  
Vol 104 (47) ◽  
pp. 18490-18495 ◽  
Author(s):  
N. Declerck ◽  
L. Bouillaut ◽  
D. Chaix ◽  
N. Rugani ◽  
L. Slamti ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document