Regulation of uptake and processing of the quorum-sensing autoinducer AI-2 in Escherichia coli
Regulation of uptake and processing of the quorum-sensing autoinducer AI-2 in Escherichia coli
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DOI：
10.1128/jb.187.1.238-248.2005
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发表时间：
2005-01-01
影响因子：
3.2
通讯作者：
Bassler, BL
中科院分区：
文献类型：
--
作者：
Xavier, KB;Bassler, BL
AI-2是一种群体感应信号分子，被认为参与种间通讯。在大肠杆菌和鼠伤寒沙门氏菌中，细胞外AI-2在指数期积累，但进入稳定期后数量急剧下降。In S.肠血清型鼠伤寒沙门氏菌，活性的降低是由于输入和加工AI-2的LSR转运蛋白。我们发现LSR转运蛋白在大肠杆菌中是有功能的。coli中筛选AI-2内化缺陷的突变体，发现lsrK和glpD。与野生型不同，lsrK和glpD突变体不激活响应AI-2的lsr操纵子的转录。lsrK编码AI-2激酶，并且lsrK突变体不能激活lsr表达，因为它不能产生磷酸-AI-2，磷酸-AI-2是lsr操纵子诱导剂。glpD编码甘油-3-磷酸（G3 P）脱氢酶，其参与甘油和G3 P代谢。G3 P在glpD突变体中积累，并通过阻止环腺苷酸（cAMP）-分解代谢物激活蛋白（CAP）依赖性激活来抑制lsr转录。二羟基丙酮磷酸（DHAP）也积累在glpD突变体，和DHAP抑制lsr转录的cAMP-CAP-独立的机制，涉及LsrR，lsr操纵子阻遏。lsr激活中对cAMP-CAP的需求解释了为什么AI-2在含有引起分解代谢物抑制的糖的培养基中生长的细菌的培养液中持续存在。这些发现表明，根据当时的生长条件，AI-2信号存在的时间以及给定细菌群落保持暴露于该信号的时间可能会有很大差异。
AI-2 is a quorum-sensing signaling molecule proposed to be involved in interspecies communication. In Escherichia coli and Salmonella enterica serovar Typhimurium, extracellular AI-2 accumulates in exponential phase, but the amount decreases drastically upon entry into stationary phase. In S. enterica serovar Typhimurium, the reduction in activity is due to import and processing of AI-2 by the Lsr transporter. We show that the Lsr transporter is functional in E. coli, and screening for mutants defective in AI-2 internalization revealed lsrK and glpD. Unlike the wild type, lsrK and glpD mutants do not activate transcription of the lsr operon in response to AI-2. lsrK encodes the AI-2 kinase, and the lsrK mutant fails to activate lsr expression because it cannot produce phospho-AI-2, which is the lsr operon inducer. glpD encodes the glycerol-3-phosphate (G3P) dehydrogenase, which is involved in glycerol and G3P metabolism. G3P accumulates in the glpD mutant and represses lsr transcription by preventing cyclic AMP (cAMP)-catabolite activator protein (CAP)-dependent activation. Dihydroxyacetone phosphate (DHAP) also accumulates in the glpD mutant, and DHAP represses lsr transcription by a cAMP-CAP-independent mechanism involving LsrR, the lsr operon repressor. The requirement for cAMP-CAP in lsr activation explains why AI-2 persists in culture fluids of bacteria grown in media containing sugars that cause catabolite repression. These findings show that, depending on the prevailing growth conditions, the amount of time that the AI-2 signal is present and, in turn, the time that a given community of bacteria remains exposed to this signal can vary greatly.