The virulence regulator sae of Staphylococcus aureus:: Promoter activities and response to phagocytosis-related signals
The virulence regulator sae of Staphylococcus aureus:: Promoter activities and response to phagocytosis-related signals
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DOI：
10.1128/jb.01927-07
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发表时间：
2008-05-01
影响因子：
3.2
通讯作者：
Wolz, Christiane
中科院分区：
文献类型：
--
作者：
Geiger, Tobias;Goerke, Christiane;Wolz, Christiane
金黄色葡萄球菌的双组分系统SAERRS与主要毒力因子的调控密切相关。然而，人们对导致SAESRS激活的信号知之甚少。在SAE操纵子中表达了来自三个不同转录起点的四个重叠的转录本(T1到T4)。我们使用P-半乳糖苷酶报告基因分析来鉴定saeRS上游区域内的可能的启动子区域。主要转录本T2可能是通过对T1转录本进行内切核处理而产生的。在saeRS上游区域只检测到两个不同的启动子元件(P1和P3)。P3启动子位于saeRS的上游，产生T3转录本，包括一个顺式作用的增强子元件，并被saeRS抑制。最远端的P1启动子被AGR强烈地自我调节，被AGR激活，并被Sigma因子B抑制。在Newman株中，组氨酸激酶SAES内的一个突变导致一个结构性激活的SAE系统。不同外界信号的比较表明，菌株ISP479R和菌株UAMS-1中的PI启动子被低pH和高盐浓度抑制，但被过氧化氢激活。除ISP479R和Col菌株外，在α-防御素的亚抑制浓度下，金黄色葡萄球菌的PI诱导最为显著。抗菌肽LL37和达托霉素不能激活P1。综上所述，这些结果表明，感受器分子SAEs是通过膜内的变化激活的，允许病原体对吞噬相关的效应分子发生反应。
The two-component system SaeRS of Staphylococcus aureus is closely involved in the regulation of major virulence factors. However, little is known about the signals leading to saeRS activation. A total of four overlapping transcripts (T1 to T4) from three different transcription starting points are expressed in the sae operon. We used a P-galactosidase reporter assay to characterize the putative promoter regions within the saeRS upstream region. The main transcript T2 is probably generated by endoribonucleolytic processing of the T1 transcript. Only two distinct promoter elements (P1 and P3) could be detected within the saeRS upstream region. The P3 promoter, upstream of saeRS, generates the T3 transcript, includes a cis-acting enhancer element and is repressed by saeRS. The most distal P1 promoter is strongly autoregulated, activated by agr, and repressed by sigma factor B. In strain Newman a mutation within the histidine kinase SaeS leads to a constitutively activated sae system. Evaluation of different external signals revealed that the PI promoter in strain ISP479R and strain UAMS-1 is inhibited by low pH and high NaCl concentrations but activated by hydrogen peroxide. The most prominent induction of PI was observed at subinhibitory concentrations of alpha-defensins in various S. aureus strains, with the exception of strain ISP479R and strain COL. P1 was not activated by the antimicrobial peptides LL37 and daptomycin. In summary, the results indicate that the sensor molecule SaeS is activated by alteration within the membrane allowing the pathogen to react to phagocytosis related effector molecules.