The arl locus positively regulates Staphylococcus aureus type 5 capsule via an mgrA-dependent pathway

Luong, Thanh T.; Lee, Chia Y.

doi:10.1099/mic.0.29177-0

Cited by 85 publications

(85 citation statements)

References 35 publications

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“…Although capsule production is very important in the survival of S. aureus during different phases of infection, very little is known about the mechanism that regulates the cap operon. Several global regulators have been shown to affect the production of the capsule, indicating that several environmental and host signals must be integrated to fine-tune this process (Luong et al, , 2003(Luong et al, , 2011Luong & Lee, 2006;Chen et al, 2007;Dassy et al, 1993;Gupta et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

“…Several global regulators have been shown to control the production of the capsule, including agr, sarA, arl and mgrA, as well as others (Luong et al, , 2003(Luong et al, , 2011Luong & Lee, 2006;Chen et al, 2007;Dassy et al, 1993;Gupta et al, 2013). A detailed analysis of the cap operon promoter has revealed that it is highly regulated (Ouyang et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

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MsaB activates capsule production at the transcription level in Staphylococcus aureus

2016

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Staphylococcus aureus produces several virulence factors that allow it to cause a variety of infections. One of the major virulence factors is the capsule, which contributes to the survival of the pathogen within the host as a way to escape phagocytosis. The production of the capsular polysaccharide is encoded in a 16 gene operon, which is regulated in response to several environmental stimuli including nutrient availability. For instance, the capsule is produced in the late-and post-exponential growth phases, but not in the early-or mid-exponential growth phase. Several regulators are involved in capsule production, but the regulation of the cap operon is still poorly understood. In this study, we show that MsaB activates the cap operon by binding directly to a 10 bp repeat in the promoter region. We show that despite the fact that MsaB is expressed throughout four growth phases, it only activates capsule production in the late-and post-exponential growth phases. Furthermore, we find that MsaB does not bind to its target site in the early and mid-exponential growth phases. This correlates with decreased nutrient availability and capsule production. These data suggest either that MsaB binding ability changes in response to nutrients or that other cap operon regulators interfere with the binding of MsaB to its target site. This study increases our understanding of the regulation of capsule production and the mechanism of action of MsaB.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MsaB activates capsule production at the transcription level in Staphylococcus aureus

2016

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“…We checked that the agrA mutant showed a phenotype similar to that of the agrCA mutant. The DNA fragment of apsR or agrA amplified with specific primers was cloned into pCL15, an E. coli-S. aureus shuttle vector with a Pspac promoter (Luong & Lee, 2006). The plasmid was electroporated into RN4220.…”

Section: Methodsmentioning

confidence: 99%

Growth-phase dependence of susceptibility to antimicrobial peptides in Staphylococcus aureus

et al. 2011

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Bacterial cell surface charge is responsible for susceptibility to cationic antimicrobial peptides. Previously, Staphylococcus aureus dlt and mprF were identified as factors conferring a positive charge upon cell surfaces. In this study, we investigated the regulation of cell surface charge during growth. Using a group of S. aureus MW2 mutants, which are gene-inactivated in 15 types of two-component systems (TCSs), we tested dltC and mprF expression and found that two TCSs, aps and agr, were associated with dltC and mprF expression in a growth phase-dependent manner. The first of these, aps, which had already been identified as a sensor of antimicrobial peptides and a positive regulator of dlt and mprF expression, was expressed strongly in the exponential phase, while its expression was significantly suppressed by agr in the stationary phase, resulting in higher expression of dltC and mprF in the exponential phase and lower expression in the stationary phase. Since both types of expression affected the cell surface charge, the susceptibility to antimicrobial peptides and cationic antibiotics was changed during growth. Furthermore, we found that the ability to sense antimicrobial peptides only functioned in the exponential phase. These results suggest that cell surface charge is tightly regulated during growth in S. aureus. INTRODUCTIONStaphylococcus aureus is a well-known major pathogen in humans. S. aureus produces many toxins and exoenzymes to cause various suppurative diseases, food poisoning and toxic shock syndrome (Foster, 2004;Lowy, 1998;Manders, 1998). Furthermore, strains isolated clinically, especially meticillin-resistant S. aureus (MRSA), exhibit multiple antibiotic resistance (Deurenberg et al., 2007;Grundmann et al., 2006), resulting in serious problems with regard to therapy of S. aureus infectious disease. Recently, besides these virulence factors, S. aureus has also been found to possess the ability to produce several factors that protect against host-derived innate immune factors, such as complement, antibodies and neutrophils, as well as recently recognized innate immune antimicrobial peptides, such as LL-37 and defensins (Foster, 2005;Rooijakkers et al., 2005).Human antimicrobial peptides are one of the innate immune factors and are produced in various tissues and organs, such as the skin, lung and intestines (Ganz et al., 1985;Ganz & Lehrer, 1995;Lehrer & Ganz, 1999;Selsted & Ouellette, 2005;Zaiou & Gallo, 2002). The most wellknown antimicrobial peptides are the defensins. Defensins are classified into two types: alpha-defensins from neutrophils and Paneth cells, and beta-defensins from epithelial cells (Cunliffe, 2003;Ganz et al., 1985;Ganz & Lehrer, 1995). Another major peptide is CAP18/LL37, which is found in neutrophils and epithelial cells (Larrick et al., 1995;Ramanathan et al., 2002;Zaiou & Gallo, 2002). These cationic peptides are electrostatically attracted to bacterial cell surfaces. Then, the peptides interact with membrane lipids, causing membrane permeabilization and leading to ...

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“…The transposon was transduced to Newman and 10833 using phage 80 as described by Kasatiya & Baldwin (1967). For complementation of the mutation, aur from 10833 or Newman was cloned into the IPTGinducible vector pCL15 (Luong & Lee, 2006). Primers aur-pCL15Fwd (59-GTGAGGAAATTTTCAAGATATG-39) and aur-pCL15Rev (59-TTACTCCACGCCTACTTCATTCC-39) were used to amplify the aur gene from 10833 or Newman genomic DNA.…”

Section: Methodsmentioning

confidence: 99%

Staphylococcus aureus clumping factor B mediates biofilm formation in the absence of calcium

Abraham

Jefferson

2012

Microbiology

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The arl locus positively regulates Staphylococcus aureus type 5 capsule via an mgrA-dependent pathway

Cited by 85 publications

References 35 publications

MsaB activates capsule production at the transcription level in Staphylococcus aureus

MsaB activates capsule production at the transcription level in Staphylococcus aureus

Growth-phase dependence of susceptibility to antimicrobial peptides in Staphylococcus aureus

Staphylococcus aureus clumping factor B mediates biofilm formation in the absence of calcium

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