Mitra Arindam, Herren Christopher D, Patel Isha R, Coleman Adam, Mukhopadhyay Suman
Virginia-Maryland Regional College of Veterinary Medicine, University of Maryland, College Park, Maryland, United States of America.
PLoS One. 2016 Jun 30;11(6):e0157532. doi: 10.1371/journal.pone.0157532. eCollection 2016.
The quorum sensing molecule Autoinducer-2 (AI-2) is generated as a byproduct of activated methyl cycle by the action of LuxS in Escherichia coli. AI-2 is synthesized, released and later internalized in a cell-density dependent manner. Here, by mutational analysis of the genes, uvrY and csrA, we describe a regulatory circuit of accumulation and uptake of AI-2. We constructed a single-copy chromosomal luxS-lacZ fusion in a luxS + merodiploid strain and evaluated its relative expression in uvrY and csrA mutants. At the entry of stationary phase, the expression of the fusion and AI-2 accumulation was positively regulated by uvrY and negatively regulated by csrA respectively. A deletion of csrA altered message stability of the luxS transcript and CsrA protein exhibited weak binding to 5' luxS regulatory region. DNA protein interaction and chromatin immunoprecipitation analysis confirmed direct interaction of UvrY with the luxS promoter. Additionally, reduced expression of the fusion in hfq deletion mutant suggested involvement of small RNA interactions in luxS regulation. In contrast, the expression of lsrA operon involved in AI-2 uptake, is negatively regulated by uvrY and positively by csrA in a cell-density dependent manner. The dual role of csrA in AI-2 synthesis and uptake suggested a regulatory crosstalk of cell signaling with carbon regulation in Escherichia coli. We found that the cAMP-CRP mediated catabolite repression of luxS expression was uvrY dependent. This study suggests that luxS expression is complex and regulated at the level of transcription and translation. The multifactorial regulation supports the notion that cell-cell communication requires interaction and integration of multiple metabolic signals.
群体感应分子自诱导物-2(AI-2)是大肠杆菌中LuxS作用于活性甲基循环产生的副产物。AI-2以细胞密度依赖性方式合成、释放并随后内化。在此,通过对uvrY和csrA基因的突变分析,我们描述了AI-2积累和摄取的调控回路。我们在luxS + 部分二倍体菌株中构建了单拷贝染色体luxS-lacZ融合体,并评估了其在uvrY和csrA突变体中的相对表达。在稳定期开始时,融合体的表达和AI-2积累分别受到uvrY的正调控和csrA的负调控。csrA的缺失改变了luxS转录本的信息稳定性,并且CsrA蛋白与luxS 5'调控区域的结合较弱。DNA-蛋白质相互作用和染色质免疫沉淀分析证实了UvrY与luxS启动子的直接相互作用。此外,hfq缺失突变体中融合体表达的降低表明小RNA相互作用参与了luxS调控。相反,参与AI-2摄取的lsrA操纵子的表达在细胞密度依赖性方式下受到uvrY的负调控和csrA的正调控。csrA在AI-2合成和摄取中的双重作用表明大肠杆菌中细胞信号传导与碳代谢调控之间存在调控串扰。我们发现cAMP-CRP介导的luxS表达的分解代谢物阻遏是uvrY依赖性的。这项研究表明luxS表达是复杂的,并且在转录和翻译水平上受到调控。多因素调控支持了细胞间通讯需要多种代谢信号相互作用和整合的观点。