Hu Xuchen, Wang Yuxia, Gao Li, Jiang Wenxin, Lin Wenzhen, Niu Chenguang, Yuan Keyong, Ma Rui, Huang Zhengwei
Department of Endodontics, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology, National Clinical Research Center of Stomatology, Shanghai, China.
Department of Endodontics, Tianjin Stomatological Hospital, Nankai University, Tianjin, China.
Front Microbiol. 2018 Mar 12;9:404. doi: 10.3389/fmicb.2018.00404. eCollection 2018.
The gene is present in a wide range of bacteria and is involved in many cellular processes. LuxS mutation can cause autoinducer(AI)-2 deficiency and methyl metabolism disorder. The objective of this study was to demonstrate that, in addition to AI-2-mediated quorum sensing (QS), methyl metabolism plays an important role in LuxS regulation in . The gene from was amplified and introduced into the -null strain to complement the methyl metabolism disruption in a defective QS phenotype. The intracellular activated methyl cycle (AMC) metabolites [S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), homocysteine (HCY), and methionine] were quantified in wild-type and its three derivatives to determine the metabolic effects of disrupting the AMC. Biofilm mass and structure, acid tolerance, acid production, exopolysaccharide synthesis of multispecies biofilms and the transcriptional level of related genes were determined. The results indicated that SAH and SAM were relatively higher in -null strain and null strain with plasmid pIB169 when cultured overnight, and HCY was significantly higher in UA159. Consistent with the transcriptional profile, deletion-mediated impairment of biofilm formation and acid tolerance was restored to wild-type levels using transgenic SahH. These results also suggest that methionine methyl metabolism contributes to LuxS regulation in to a significant degree.
该基因存在于多种细菌中，并参与许多细胞过程。LuxS突变可导致自诱导物（AI）-2缺乏和甲基代谢紊乱。本研究的目的是证明，除了AI-2介导的群体感应（QS）外，甲基代谢在[具体细菌名称未给出]的LuxS调控中也起着重要作用。从[具体细菌名称未给出]扩增该基因并将其导入[具体细菌名称未给出]基因缺失菌株，以弥补有缺陷的QS表型中的甲基代谢破坏。在野生型[具体细菌名称未给出]及其三种衍生物中对细胞内活化甲基循环（AMC）代谢物[S-腺苷甲硫氨酸（SAM）、S-腺苷同型半胱氨酸（SAH）、同型半胱氨酸（HCY）和甲硫氨酸]进行定量，以确定破坏AMC的代谢效应。测定了多物种生物膜的生物膜量和结构、耐酸性、产酸、胞外多糖合成以及相关基因的转录水平。结果表明，过夜培养时，在[具体细菌名称未给出]基因缺失菌株和携带质粒pIB169的[具体细菌名称未给出]基因缺失菌株中，SAH和SAM相对较高，而在[具体细菌名称未给出]UA159中HCY显著较高。与转录谱一致，使用转基因SahH可将[具体细菌名称未给出]缺失介导的生物膜形成和耐酸性损伤恢复到野生型水平。这些结果还表明，甲硫氨酸甲基代谢在很大程度上有助于[具体细菌名称未给出]中的LuxS调控。
