Staphylococcus aureus AI-2 Quorum Sensing Associates with the KdpDE Two-Component System To Regulate Capsular Polysaccharide Synthesis and Virulence
Staphylococcus aureus AI-2 Quorum Sensing Associates with the KdpDE Two-Component System To Regulate Capsular Polysaccharide Synthesis and Virulence
复制标题
金黄色葡萄球菌 AI-2 群体感应与 KdpDE 双组分系统结合调节荚膜多糖合成和毒力
DOI：
10.1128/iai.00131-10
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发表时间：
2010-08-01
影响因子：
3.1
通讯作者：
Sun, Baolin
中科院分区：
文献类型：
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作者：
Zhao, Liping;Xue, Ting;Sun, Baolin
自诱导剂2 （Autoinducer 2, AI-2）被广泛认为是革兰氏阴性菌种内和种间通讯的信号分子，但其在革兰氏阳性菌，尤其是金黄色葡萄球菌中的信号功能尚不清楚。本研究揭示了LuxS在金黄色葡萄球菌NCTC8325中调控荚膜多糖合成的作用，并表明AI-2作为信号分子可以调控基因表达，参与金黄色葡萄球菌的一些生理活动。luxS在金黄色葡萄球菌NCTC8325中的失活导致荚膜多糖合成基因的转录水平升高。luxS突变体在人血和U937巨噬细胞中的存活率均高于野生型。与luxS突变体相比，添加化学合成的AI-2前体分子4,5-二羟基-2,3-戊二酮（DPD）的培养物恢复了所有亲本表型，表明AI-2在金黄色葡萄球菌中具有信号功能。此外，我们证明LuxS/AI-2信号系统通过双组分系统KdpDE调节荚膜多糖的产生，该系统在金黄色葡萄球菌中的功能尚未明确。这种调节是通过KdpE与帽启动子结合的磷酸化发生的。
ABSTRACT Autoinducer 2 (AI-2) is widely recognized as a signal molecule for intra- and interspecies communication in Gram-negative bacteria, but its signaling function in Gram-positive bacteria, especially in Staphylococcus aureus, remains obscure. Here we reveal the role of LuxS in the regulation of capsular polysaccharide synthesis in S. aureus NCTC8325 and show that AI-2 can regulate gene expression and is involved in some physiological activities in S. aureus as a signaling molecule. Inactivation of luxS in S. aureus NCTC8325 resulted in higher levels of transcription of capsular polysaccharide synthesis genes. The survival rate of the luxS mutant was higher than that of the wild type in both human blood and U937 macrophages. In comparison to the luxS mutant, a culture supplemented with chemically synthesized 4,5-dihydroxy-2,3-pentanedione (DPD), the AI-2 precursor molecule, restored all the parental phenotypes, suggesting that AI-2 has a signaling function in S. aureus. Furthermore, we demonstrated that the LuxS/AI-2 signaling system regulates capsular polysaccharide production via a two-component system, KdpDE, whose function has not yet been clarified in S. aureus. This regulation occurred via the phosphorylation of KdpE binding to the cap promoter.