The luxS gene is involved in cell-cell signalling for toxin production in Clostridium perfringens
The luxS gene is involved in cell-cell signalling for toxin production in Clostridium perfringens
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DOI：
10.1046/j.1365-2958.2002.02863.x
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发表时间：
2002-04-01
影响因子：
3.6
通讯作者：
Shimizu, T
中科院分区：
文献类型：
--
作者：
Ohtani, K;Hayashi, H;Shimizu, T
一种革兰氏阳性厌氧病原体，产气荚膜梭菌，通过产生许多细胞外毒素和酶，共同作用降解宿主组织，从而引起梭菌肌坏死或气性坏疽。C.产气荚膜杆菌具有luxS基因的同源物，据报道该基因负责产生自身诱导物2（AI-2），其参与细菌中的群体感应。利用C.产气荚膜杆菌菌株13，并检查了luxS基因在毒素产生中的作用。野生型菌株13的无细胞培养上清对哈维氏弧菌BB 170的发光有很大的刺激作用，而luxS突变株的无细胞培养上清对哈维氏弧菌BB 170的发光没有明显的刺激作用，表明luxS基因是哈维氏弧菌产生AI-2所必需的。产气荚膜杆菌luxS突变体显示出α-、κ-和θ-毒素的产生水平降低。在luxS突变体中，θ-毒素基因（pfoA）的转录在指数生长中期较低，而α-和κ-毒素基因的转录没有受到显着影响。通过添加来自野生型细胞的培养上清液刺激luxS突变体中毒素的产生，这可能是因为AI-2的存在。此外，当在野生型C.产气荚膜梭菌、大肠杆菌DH 5 α携带C.产气荚膜杆菌对luxS操纵子的缺失分析表明，luxS基因单独负责细胞-细胞信号传导，并且位于luxS上游的metB或cysK基因不参与调节毒素产生。我们的研究结果表明，AI-2的细胞-细胞信号在调节C.产气荚膜杆菌
A Gram-positive anaerobic pathogen, Clostridium perfringens , causes clostridial myonecrosis or gas gangrene in humans by producing numerous extracellular toxins and enzymes that act in concert to degrade host tissues. C. perfringens possesses a homologue of the luxS gene that is reported to be responsible for the production of autoinducer 2 (AI-2), which participates in quorum sensing in bacteria. The luxS mutant was constructed using C. perfringens strain 13, and the role of the luxS gene in toxin production was examined. The cell-free culture supernatant from wild-type strain 13 greatly stimulated the luminescence of Vibrio harveyi BB170, whereas that from the luxS mutant caused no significant stimulation, indicating that the luxS gene is necessary for AI-2 production in C. perfringens . The luxS mutant showed a reduced level of production of alpha-, kappa- and theta-toxins. In the luxS mutant, the transcription of the theta-toxin gene (pfoA ) was lower at mid-exponential growth phase, whereas alpha- and kappa-toxin gene transcription was not significantly affected. The production of toxins in the luxS mutant was stimulated by the addition of the culture supernatant from the wild-type cells, possibly because of the presence of AI-2. Moreover, the expression of the pfoA gene in the luxS mutant was apparently activated when the mutant cells were cultured in the presence of culture supernatants from the wild-type C. perfringens , Escherichia coli DH5alpha carrying the luxS gene of C. perfringens. A deletion analysis of the luxS operon showed that the luxS gene alone is responsible for cell-cell signalling, and that the metB or cysK genes located upstream of luxS are not involved in regulating toxin production. Our results indicate that cell-cell signalling by AI-2 plays an important role in the regulation of toxin production in C. perfringens .