Shigella flexneri LuxS quorum-sensing system modulates virB expression but is not essential for virulence
Shigella flexneri LuxS quorum-sensing system modulates virB expression but is not essential for virulence
复制标题
DOI：
10.1128/iai.69.1.15-23.2001
复制
发表时间：
2001-01-01
影响因子：
3.1
通讯作者：
Maurelli, AT
中科院分区：
文献类型：
--
作者：
Day, WA;Maurelli, AT
群体感应系统调节各种植物和动物病原体中毒力因子的表达，包括肠杆菌科的成员。对志贺氏菌毒力基因表达的研究表明，在高细胞密度下，这种毒力细胞器的III型分泌系统及其底物编码基因的最高表达和最大活性发生。在这些研究中，我们证明了IPA、MXI和SpA入侵操纵子在固定相细菌中的表达是最大的，来自固定相培养的条件培养液增强了这些基因的表达。相反，Virb的表达在对数晚期达到高峰，Virb是表达侵袭基因所必需的转录因子；因此，Virb的表达被来自对数晚期培养的条件培养液中存在的信号(S)增强。自体诱导物2(AI-2)是志贺氏菌和肠侵袭性大肠杆菌合成的一种在对数末期活跃的仲裁信号分子，与VIRB的表达高峰有关。然而，AI-2不影响入侵操纵子的表达，也不是志贺氏菌毒力所必需的，因为缺乏AI-2合成的突变株是完全毒力的。讨论了这些发现对VIRB和侵袭操纵子表达的影响，以及控制毒力基因表达的回路的进化。
Quorum-sensing systems regulate the expression of virulence factors in a wide variety of plant and animal pathogens, including members of the Enterobacteriaceae. Studies of Shigella virulence gene expression have demonstrated that maximal expression of genes encoding the type III secretion system and its substrates and maximal activity of this virulence organelle occur at high cell density. In these studies, we demonstrate that the expression of ipa, mxi, and spa invasion operons is maximal in stationary-phase bacteria and that conditioned media derived from stationary-phase cultures enhance the expression of these loci. In contrast, expression of virB, a transcription factor essential for the expression of invasion loci, peaks in late log phase; accordingly, virB expression is enhanced by a signal(s) present in conditioned media derived from late-log-phase cultures. Autoinducer 2 (AI-2), a quorum signaling molecule active in late log phase, was synthesized by Shigella species and enteroinvasive Escherichia coli and shown to be responsible for the observed peak of virB expression. However, AI-2 does not influence invasion operon expression and is not required for Shigella virulence, as mutants deficient in AI-2 synthesis are fully virulent. The implications of these findings with regard to both virB and invasion operon expression and the evolution of circuitries governing virulence gene expression are discussed.