Shao Hanjuan, James Deanna, Lamont Richard J, Demuth Donald R
Department of Periodontics, Endodontics and Dental Hygiene, University of Louisville School of Dentistry, 501 South Preston Street, Room 209, Louisville, KY 40292, USA.
J Bacteriol. 2007 Aug;189(15):5559-65. doi: 10.1128/JB.00387-07. Epub 2007 May 25.
Our previous studies showed that the Aggregatibacter actinomycetemcomitans RbsB protein interacts with cognate and heterologous autoinducer 2 (AI-2) signals and suggested that the rbsDABCK operon encodes a transporter that may internalize AI-2 (D. James et al., Infect. Immun. 74:4021-4029, 2006.). However, A. actinomycetemcomitans also possesses genes related to the lsr operon of Salmonella enterica serovar Typhimurium which function to import AI-2. Here, we show that A. actinomycetemcomitans LsrB protein competitively inhibits the interaction of the Vibrio harveyi AI-2 receptor (LuxP) with AI-2 from either A. actinomycetemcomitans or V. harveyi. Interestingly, LsrB was a more potent inhibitor of LuxP interaction with AI-2 from V. harveyi whereas RbsB competed more effectively with LuxP for A. actinomycetemcomitans AI-2. Inactivation of lsrB in wild-type A. actinomycetemcomitans or in an isogenic RbsB-deficient strain reduced the rate by which intact bacteria depleted A. actinomycetemcomitans AI-2 from solution. Consistent with the results from the LuxP competition experiments, the LsrB-deficient strain depleted AI-2 to a lesser extent than the RbsB-deficient organism. Inactivation of both lsrB and rbsB virtually eliminated the ability of the organism to remove AI-2 from the extracellular environment. These results suggest that A. actinomycetemcomitans possesses two proteins that differentially interact with AI-2 and may function to inactivate or facilitate internalization of AI-2.
我们之前的研究表明，伴放线聚集杆菌的RbsB蛋白可与同源及异源自诱导物2（AI-2）信号相互作用，并提示rbsDABCK操纵子编码一种可能使AI-2内化的转运蛋白（D. 詹姆斯等人，《感染与免疫》74:4021 - 4029，2006年）。然而，伴放线聚集杆菌也拥有与鼠伤寒沙门氏菌血清型鼠伤寒的lsr操纵子相关的基因，该操纵子的功能是导入AI-2。在此，我们表明伴放线聚集杆菌的LsrB蛋白竞争性抑制哈维弧菌AI-2受体（LuxP）与来自伴放线聚集杆菌或哈维弧菌的AI-2之间的相互作用。有趣的是，LsrB是LuxP与来自哈维弧菌的AI-2相互作用的更有效抑制剂，而RbsB与LuxP竞争伴放线聚集杆菌AI-2时更有效。在野生型伴放线聚集杆菌或同基因RbsB缺陷菌株中使lsrB失活，降低了完整细菌从溶液中消耗伴放线聚集杆菌AI-2的速率。与LuxP竞争实验的结果一致，LsrB缺陷菌株消耗AI-2的程度低于RbsB缺陷菌株。使lsrB和rbsB都失活实际上消除了该菌从细胞外环境中去除AI-2的能力。这些结果表明，伴放线聚集杆菌拥有两种与AI-2有不同相互作用的蛋白，可能起到使AI-2失活或促进其内化的作用。
