Regulation of autoinducer 2 production and luxS expression in a pathogenic Edwardsiella tarda strain
Regulation of autoinducer 2 production and luxS expression in a pathogenic Edwardsiella tarda strain
复制标题
致病性爱德华氏菌菌株中自诱导子 2 产生和 luxS 表达的调节
DOI：
10.1099/mic.0.2008/017343-0
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发表时间：
2008-07-01
期刊：
影响因子：
2.8
通讯作者：
Sun, Li
中科院分区：
文献类型：
--
作者：
Zhang, Min;Sun, Kun;Sun, Li
迟缓爱德华氏菌是一种可以感染人类和动物的细菌病原体。TX 1是从病鱼中分离的一株迟发型爱德华氏菌，它能产生类似于自诱导物2（Al-2）的活性，这种活性依赖于生长阶段，并受生长条件的调节。从TX 1中克隆了编码Al-2合酶的基因，并命名为luxS（Et）。LuxS（Et）能够补充大肠杆菌菌株DH 5 α的Al-2突变表型。luxS（Et）的表达与Al-2活性相关，且随葡萄糖浓度升高而增加，随温度升高而降低。葡萄糖的作用显示通过cAMP-CRP复合物介导，其抑制luxS（Et）表达。过表达luxS（Et）增强TX 1中Al-2活性，而通过反义RNA干扰破坏luxS（Et）表达（i）降低Al-2活性水平，（ii）在各种条件下损害细菌生长，（iii）减弱与III型分泌系统和生物膜形成相关的基因表达，（iv）减弱细菌毒力。添加外源Al-2能够弥补TTSS基因表达和生物膜产生的缺陷，但未能挽救生长缺陷。我们的结果（i）证明TX 1中的Al-2活性至少部分地在luxS（Et）表达水平上受到控制，而luxS（Et）表达又受生长条件的调节，并且luxS（Et）的瞬时表达对于最佳细菌感染和存活是必需的;和（ii）建议在Ed. tarda的LuxS/Al-2介导的信号转导途径，调节生产的毒力相关元件的存在。
Edwardsiella tarda is a bacterial pathogen that can infect both humans and animals. TX1, an Ed. tarda strain isolated from diseased fish, was found to produce autoinducer 2 (Al-2)-like activity that was growth phase dependent and modulated by growth conditions. The gene coding for the Al-2 synthase was cloned from TX1 and designated luxS(Et). LuxS(Et) was able to complement the Al-2 mutant phenotype of Escherichia coli strain DH5 alpha. Expression Of luxS(Et) correlated with Al-2 activity and was increased by glucose and decreased by elevated temperature. The effect of glucose was shown to be mediated through the cAMP-CRP complex, which repressed luxS(Et) expression. Overexpression of luxS(Et) enhanced Al-2 activity in TX1, whereas disruption of luxS(Et) expression by antisense RNA interference (i) reduced the level of Al-2 activity, (ii) impaired bacterial growth under various conditions, (iii) weakened the expression of genes associated with the type III secretion system and biofilm formation, and (iv) attenuated bacterial virulence. Addition of exogenous Al-2 was able to complement the deficiencies in the expression of TTSS genes and biofilm production but failed to rescue the growth defects. Our results (i) demonstrated that the Al-2 activity in TX1 is controlled at least in part at the level of luxS(Et) expression, which in turn is regulated by growth conditions, and that the temporal expression of luxS(Et) is essential for optimal bacterial infection and survival; and (ii) suggested the existence in Ed. tarda of a LuxS/Al-2-mediated signal transduction pathway that regulates the production of virulence-associated elements.