QsvR integrates into quorum sensing circuit to control Vibrio parahaemolyticus virulence
QsvR integrates into quorum sensing circuit to control Vibrio parahaemolyticus virulence
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QsvR 集成到群体感应电路中控制副溶血性弧菌毒力
DOI：
10.1111/1462-2920.14524
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发表时间：
2019-03-01
影响因子：
5.1
通讯作者：
Zhou, Dongsheng
中科院分区：
文献类型：
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作者：
Zhang, Yiquan;Hu, Linghui;Zhou, Dongsheng
副溶血性弧菌（Vibrio parahaemolyticus）是引起全球海产品相关性胃肠炎的主要病原菌，其完全毒力需要两种III型分泌系统（T3 SS 1和T3 SS 2）和热稳定的直接溶血素（由tdh 1和tdh 2编码）。tdh基因和T3 SS 2基因簇构成了位于染色体II上的80 kb致病岛，称为Vp-PAI。T3 SS 1和Vp-PAI的表达以群体感应（QS）依赖的方式调节，但其详细机制尚不清楚。在此，我们表明，三个因素（QS调节AphA和OpaR和AraC型转录调节QsvR）形成一个复杂的调控网络来控制T3 SS 1和Vp-PAI基因的表达。在低细胞密度（LCD），而Vp-PAI表达被抑制，T3 SS 1基因诱导的AphA，它直接结合（的操纵子区域）的exsBAD-vscBCD操纵子。在高细胞密度（HCD）下，细菌通过用OpaR替换AphA来关闭T3 SS 1表达，从而触发Vp-PAI的诱导。此外，QsvR结合到所有测试的T3 SS 1和Vp-PAI基因的调控区，以激活它们在HCD的转录。综上所述，我们的数据强调了多种QS调节剂如何通过精确控制不同生长阶段主要毒力决定因子的表达来促进副溶血性弧菌的致病性。
Vibrio parahaemolyticus, the leading cause of seafood-associated gastroenteritis worldwide, requires the two type-III secretion systems (T3SS1 and T3SS2) and a thermostable direct hemolysin (encoded by tdh1 and tdh2) for full virulence. The tdh genes and the T3SS2 gene cluster constitute an 80 kb pathogenicity island known as Vp-PAI located on the chromosome II. Expression of T3SS1 and Vp-PAI is regulated in a quorum sensing (QS)-dependent manner but its detailed mechanisms remain unknown. Herein, we show that three factors (QS regulators AphA and OpaR and an AraC-type transcriptional regulator QsvR) form a complex regulatory network to control the expression of T3SS1 and Vp-PAI genes. At low cell density (LCD), whereas Vp-PAI expression is repressed, T3SS1 genes are induced by AphA, which directly binds (an operator region of) the exsBAD-vscBCD operon. At high cell density (HCD), the bacterium turns off T3SS1 expression by replacing AphA with OpaR, triggering the induction of Vp-PAI. Furthermore, QsvR binds to the regulatory regions of all the tested T3SS1 and Vp-PAI genes to activate their transcription at HCD. Taken together, our data highlight how multiple QS regulators contribute to the pathogenicity of V. parahaemolyticus by precisely controlling the expression of major virulence determinants during different stages of growth.