Specificity grouping of the accessory gene regulator quorum-sensing system of Staphylococcus epidermidis is linked to infection

2004 ◽  
Vol 181 (3) ◽  
pp. 250-253 ◽  
Author(s):  
A. B. Carmody ◽  
Michael Otto
2004 ◽  
Vol 186 (20) ◽  
pp. 6706-6713 ◽  
Author(s):  
Linsheng Zhang ◽  
Guangyong Ji

ABSTRACT The four gene products of the accessory gene regulator (agr) P2 operon of Staphylococcus aureus assemble a quorum-sensing system: AgrA and AgrC resemble a two-component signal transduction system, and AgrB and AgrD are required to produce an autoinducing peptide. Upon activation, this quorum-sensing system positively regulates the transcription of the P2 operon as well as the P3 operon, whose transcript, RNAIII, regulates the expression of virulence genes. Four groups of S. aureus have been identified based on the agr sequences and the group-specific interaction between the autoinducing peptide and AgrC. AgrB is a transmembrane protein involved in the processing of AgrD propeptide, and its interaction with AgrD is also group specific. In this study, a series of chimeric AgrBs were constructed by swapping between group I and group II AgrBs, and these mutants were used to analyze the group-specific segment(s) in AgrB that was responsible for AgrD processing. Our results revealed that the first transmembrane α-helix and the extracellular loop 1 of group I AgrB were decisive in the specific processing of group I AgrD. In contrast, two hydrophilic segments of group II AgrB played a crucial role in the group-specific processing of group II AgrD. We also found that several chimeric AgrBs were capable of processing AgrD from both groups, suggesting that all AgrB homologues may utilize the same or a similar mechanism in the processing of AgrDs.


2020 ◽  
Vol 18 (3) ◽  
pp. 379-390 ◽  
Author(s):  
Christopher P. Gordon

The accessory gene regulator (agr) quorum-sensing system is arguably the most important regulator of staphylococcus virulence and has been the focus of tremendous interest in the development of effective therapies for pathogenic bacterial infections.


Author(s):  
Korbin H. J. West ◽  
Wenqi Shen ◽  
Emma L. Eisenbraun ◽  
Tian Yang ◽  
Joseph K. Vasquez ◽  
...  

2006 ◽  
Vol 74 (1) ◽  
pp. 488-496 ◽  
Author(s):  
Lin Xu ◽  
Hualin Li ◽  
Cuong Vuong ◽  
Viveka Vadyvaloo ◽  
Jianping Wang ◽  
...  

ABSTRACT Nosocomial infections caused by Staphylococcus epidermidis are characterized by biofilm formation on implanted medical devices. Quorum-sensing regulation plays a major role in the biofilm development of many bacterial pathogens. Here, we describe luxS, a quorum-sensing system in staphylococci that has a significant impact on biofilm development and virulence. We constructed an isogenic ΔluxS mutant strain of a biofilm-forming clinical isolate of S. epidermidis and demonstrated that luxS signaling is functional in S. epidermidis. The mutant strain showed increased biofilm formation in vitro and enhanced virulence in a rat model of biofilm-associated infection. Genetic complementation and addition of autoinducer 2-containing culture filtrate restored the wild-type phenotype, demonstrating that luxS repressed biofilm formation through a cell-cell signaling mechanism based on autoinducer 2 secretion. Enhanced production of the biofilm exopolysaccharide polysaccharide intercellular adhesin in the mutant strain is presumably the major cause of the observed phenotype. The agr quorum-sensing system has previously been shown to impact biofilm development and biofilm-associated infection in a way similar to that of luxS, although by regulation of different factors. Our study indicates a general scheme of quorum-sensing regulation of biofilm development in staphylococci, which contrasts with that observed in many other bacterial pathogens.


2014 ◽  
Vol 196 (19) ◽  
pp. 3482-3493 ◽  
Author(s):  
M. E. Olson ◽  
D. A. Todd ◽  
C. R. Schaeffer ◽  
A. E. Paharik ◽  
M. J. Van Dyke ◽  
...  

2005 ◽  
Vol 187 (15) ◽  
pp. 5301-5309 ◽  
Author(s):  
Ching Wen Tseng ◽  
George C. Stewart

ABSTRACT The accessory gene regulator (Agr) system is a quorum-sensing system of Staphylococcus aureus responsible for upregulation of certain exoprotein genes and downregulation of certain cell-wall associated proteins during the post-exponential phase of growth. The enterotoxin B (seb) determinant is upregulated by the Agr system. Agr-regulated cis elements within the seb promoter region were examined by deletion analyses of the seb promoter by a hybrid promoter approach utilizing the staphylococcal lac operon promoter. To identify the regulatory pathway for enterotoxin B expression, the seb promoter fused to the chloramphenicol acetyltransferase reporter gene was introduced into mutants of S. aureus lacking agr or different members of the Sar family of transcriptional regulators. Agr control of seb promoter activity was found to be dependent upon the presence of a functional Rot protein, and Rot was shown to be able to bind to the seb promoter. Therefore, the Agr-mediated post-exponential-phase increase in seb transcription results from the Agr system's inactivation of Rot repressor activity.


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