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首页> 外文期刊>Infection and immunity >The Staphylococcus aureus GGDEF Domain-Containing Protein, GdpS, Influences Protein A Gene Expression in a Cyclic Diguanylic Acid-Independent Manner
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The Staphylococcus aureus GGDEF Domain-Containing Protein, GdpS, Influences Protein A Gene Expression in a Cyclic Diguanylic Acid-Independent Manner

机译：金黄色葡萄球菌GGDEF结构域蛋白，GdpS，影响蛋白A基因表达的循环双鸟苷酸非依赖性。

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Staphylococcus aureus is an important human pathogen that is the principal cause of a variety of diseases, ranging from localized skin infections to life-threatening systemic infections. The success of the organism as a pathogen and its ability to cause such a wide range of infections are due to its extensive virulence factors. In this study, we identified the role of the only GGDEF domain protein (GdpS [GGDEF domain protein from Staphylococcus]) in the virulence of S. aureus NCTC8325. Inactivation of gdpS results in an alteration in the production of a range of virulence factors, such as serine and cysteine proteases, fibrinogen-binding proteins, and, specifically, protein A (Spa), a major surface protein of S. aureus. The transcript level of spa decreases eightfold in the gdpS mutant compared with the parental NCTC8325 strain. Furthermore, the transcript level of sarS, which encodes a direct positive regulator of spa, also decreases in the gdpS mutant compared with the wild type, while the transcript levels of agr, sarA, sarT, and rot display no apparent changes in the gdpS mutant, suggesting that GdpS affects the expression of spa through interaction with SarS by unknown mechanisms. Furthermore, the complementation assays show that the influences of GdpS on spa and sarS depend on its N-terminal domain, which is predicted to be the sensor of a two-component system, rather than its C-terminal GGDEF domain with conserved GGDEF, suggesting that GdpS functions in S. aureus by an unknown mechanism independent of 3′,5′-cyclic diguanylic acid signaling.
机译：金黄色葡萄球菌是一种重要的人类病原体，是导致多种疾病的主要原因，从局部皮肤感染到威胁生命的全身感染。生物体作为病原体的成功及其引起如此广泛感染的能力归因于其广泛的毒力因子。在这项研究中，我们确定了唯一的GGDEF域蛋白（来自葡萄球菌< / em>]）。金黄色的 NCTC8325。 gdpS 的失活导致一系列毒力因子产生的改变，例如丝氨酸和半胱氨酸蛋白酶，纤维蛋白原结合蛋白，特别是主要表面蛋白A（Spa）的 S。金黄色。与亲本NCTC8325菌株相比， gdpS 突变体中 spa 的转录水平降低了八倍。此外，与野生型相比， gdpS 突变体中编码 spa 的直接正向调节子的 sarS 的转录水平也有所降低，而 agr ， sarA ， sarT 和 rot 的转录水平在中没有明显变化gdpS 突变体，表明GdpS通过未知机制与SarS相互作用影响 spa 的表达。此外，互补分析表明，GdpS对 spa 和 sarS 的影响取决于其N末端结构域，这被认为是两组分系统的传感器，而不是其C端GGDEF结构域具有保守的GGDEF，这表明GdpS在 S中起作用。不依赖于3'，5'-环二鸟苷酸信号传导的未知机制

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