Choi Hyun Kyung, Park Na Young, Kim Dae-il, Chung Hee Jong, Ryu Sangryeol, Choi Sang Ho
Department of Food Science and Technology, Institute of Biotechnology, Chonnam National University, Kwang-Ju, South Korea.
J Biol Chem. 2002 Dec 6;277(49):47292-9. doi: 10.1074/jbc.M206893200. Epub 2002 Sep 27.
Cytolytic hemolysin, a gene product of vvhA, is a putative virulence factor of the pathogenic bacterium Vibrio vulnificus. We have previously shown that hemolysin production is repressed by adding glucose to culture media and that production can be restored by adding cAMP. In this study, hemolysin activity and the level of vvh transcript were determined to reach a maximum in late exponential phase and were repressed when cells entered stationary phase. Northern blot and primer extension analyses revealed that vvhA is cotranscribed with a second gene, vvhB, located upstream of vvhA. Transcription of the vvhBA operon begins at a single site and is under the direction of a single promoter, P(vvh). A crp null mutation decreased hemolysin production and the level of vvhBA transcript by reducing the activity of P(vvh), indicating that the P(vvh) activity is under the positive control of cAMP receptor protein (CRP). A direct interaction between CRP and the regulatory region of the vvhBA operon was demonstrated by gel-mobility shift assays. The CRP binding site, centered at 59.5 bp upstream of the transcription start site, was mapped by deletion analysis of the vvhBA promoter region and confirmed by DNase I protection assays. These results demonstrate that the vvhBA expression is activated by CRP in a growth-dependent manner and that CRP exerts its effects by directly binding to DNA upstream of P(vvh).
溶细胞性溶血素是创伤弧菌致病细菌的vvhA基因产物,是一种假定的毒力因子。我们之前已经表明,向培养基中添加葡萄糖会抑制溶血素的产生,而添加cAMP可恢复其产生。在本研究中,溶血素活性和vvh转录水平在指数后期达到最大值,当细胞进入稳定期时受到抑制。Northern印迹和引物延伸分析表明,vvhA与位于vvhA上游的第二个基因vvhB共转录。vvhBA操纵子的转录起始于单个位点,并受单个启动子P(vvh)的指导。crp基因敲除突变通过降低P(vvh)的活性降低了溶血素的产生和vvhBA转录水平,表明P(vvh)的活性受cAMP受体蛋白(CRP)的正调控。凝胶迁移率变动分析证明了CRP与vvhBA操纵子调控区域之间的直接相互作用。通过对vvhBA启动子区域的缺失分析定位了以转录起始位点上游59.5 bp为中心的CRP结合位点,并通过DNase I保护试验得到证实。这些结果表明,vvhBA的表达由CRP以生长依赖的方式激活,并且CRP通过直接结合到P(vvh)上游的DNA发挥其作用。