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− | <h1>Quorum sensing of <i>Staphylococcus aureus</i></h1> | + | <div class="para"> |
− | + | <h1>Quorum sensing of <i>Staphylococcus aureus</i></h1> | |
− | + | <p style="font-size:20px;"> | |
− | + | <i>Staphylococcus aureus</i> is an opportunistic and invasive pathogen that utilizes quorum sensing (QS), | |
− | + | a cell-to-cell signaling mechanism, to strengthen its ability to cause disease in humans. QS allows <i>S. aureus</i> to monitor their surroundings and population size, and regulate the production of virulence factors. As shown | |
− | + | in Fig. 1, QS in <i>S. aureus </i>is regulated by the <i>agr</i> operon which consists of two transcription | |
− | + | units <i>agr</i>BDCA and RNAIII. The genes <i>agr</i>BDCA are controlled by an inducible promoter termed | |
− | + | P2. When regulatory proteins bind to P2, these four genes start to be transcribed and then translated to | |
− | + | give four different proteins which are the transmembrane protein AgrB, the precursor peptide AgrD, the receptor | |
− | + | protein AgrC and the regulator protein AgrA. The agrD encodes precursor peptides and will be post-transcriptionally | |
− | + | processed by AgrB to generate a functional QS signal molecule auto-inducing peptides (AIPs) (George and Muir, | |
− | + | 2007). When AIPs are secreted from the cells into the external environment, it can be detected by AgrC present | |
− | + | on the <i>S. aureus</i> cell surface. The binding of AIP to AgrC phosphorylates AgrA which has a higher affinity | |
− | + | to interact with P2 than the un-phosphorylated form (Koenig et al., 2004). Upon binding to the P2 promoter, | |
− | + | AgrA upregulates the transcription of the <i>agr</i> gene and leads to a higher production of AIP. | |
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+ | <figcaption><strong>Figure 1 The agr system. The arrows with a filled head show the positive feedback loop.</strong></figcaption> | ||
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Revision as of 14:00, 4 October 2017
Detection
Quorum sensing of Staphylococcus aureus
Staphylococcus aureus is an opportunistic and invasive pathogen that utilizes quorum sensing (QS), a cell-to-cell signaling mechanism, to strengthen its ability to cause disease in humans. QS allows S. aureus to monitor their surroundings and population size, and regulate the production of virulence factors. As shown in Fig. 1, QS in S. aureus is regulated by the agr operon which consists of two transcription units agrBDCA and RNAIII. The genes agrBDCA are controlled by an inducible promoter termed P2. When regulatory proteins bind to P2, these four genes start to be transcribed and then translated to give four different proteins which are the transmembrane protein AgrB, the precursor peptide AgrD, the receptor protein AgrC and the regulator protein AgrA. The agrD encodes precursor peptides and will be post-transcriptionally processed by AgrB to generate a functional QS signal molecule auto-inducing peptides (AIPs) (George and Muir, 2007). When AIPs are secreted from the cells into the external environment, it can be detected by AgrC present on the S. aureus cell surface. The binding of AIP to AgrC phosphorylates AgrA which has a higher affinity to interact with P2 than the un-phosphorylated form (Koenig et al., 2004). Upon binding to the P2 promoter, AgrA upregulates the transcription of the agr gene and leads to a higher production of AIP.