2017.03.27,我院孫寶林教授研究組和蔡剛教授研究組合作在 International Journal of Medical Microbiology 發(fā)表研究論文:AI-2 quorum sensing negatively regulates rbf expression and biofilm formation in Staphylococcus aureus
作 者: Ronghua Ma, Shuwan Qiu, Qiu Jiang, Haipeng Sun, Ting Xue, Gang Cai, Baolin Sun
Abstract:Staphylococcus aureus is an important pathogen that is capable of forming biofilms on biomaterial surfaces to cause biofilm-associated infections. Autoinducer 2 (AI-2), a universal language for interspecies communication, is involved in a variety of physiological activities, although its exact role in Gram-positive bacteria, especially in S. aureus, is not yet thoroughly characterized. Herein we demonstrate that inactivation of luxS, which encodes AI-2 synthase, resulted in increased biofilm formation and higher polysaccharide intercellular adhesion (PIA) production compared with the wild-type strain in S. aureus NCTC8325. The transcript level of rbf, a positive regulator of biofilm formation, was significantly increased in the luxS mutant. All of the parental phenotypes could be restored by genetic complementation and chemically synthesized 4,5-dihydroxy-2,3-pentanedione, the AI-2 precursor molecule,? suggesting that AI-2 has a signaling function to regulate rbf transcription and biofilm formation in S. aureus. Furthermore, phenotypic analysis revealed that the luxS rbf double mutant produced approximately the same amount of biofilms and PIA as the rbf mutant. In addition, real-time RT-PCR analysis showed that the icaA transcript level of the rbf mutant was similar to that of the luxS rbf double mutant. These findings demonstrate that the LuxS/AI-2 system regulates PIA-dependent biofilm formation via repression of rbf expression in S. aureus. In addition, we demonstrated that Rbf could bind to the sarX and rbf promoters to upregulate their expression.
版權與免責聲明:本網(wǎng)頁的內容由收集互聯(lián)網(wǎng)上公開發(fā)布的信息整理獲得。目的在于傳遞信息及分享,并不意味著贊同其觀點或證實其真實性,也不構成其他建議。僅提供交流平臺,不為其版權負責。如涉及侵權,請聯(lián)系我們及時修改或刪除。郵箱:sales@allpeptide.com