Cell-Cell Communication And Signal Transduction In Escherichia Coli

In the life span of bacteria, environmental cues, density of bacteria and physiological states keep changing. To respond to these variable conditions, bacteria have learned how to use small molecular as signal, and evolved a variety of signal sensing and delivering mechanisms during the long evolution progress. Cell-to-cell communication in bacteria that leads to co-ordinated behaviour at a multicellular level is often referred to as quorum sensing, or density-dependent gene regulation, in this process bacteria produce, release and respond to signaling molecules called autoinducers. While bacteria proliferated, autoinducers accumulated in the around environment, once reached a threshold autoinducers can be detected and enter the cell, bind to its receptors and regulate transcription of lots of target genes. Escherichia coli K-12 has two kinds of quorum sensing systems, system 1 which uses AI-1 as signal molecular, and system 2 which uses AI-2 as signal molecular.Quorum sensing system 1 includes protein pairs similar to LuxR and LuxI. The system 1 autoinducer named AM is produced by LuxI and is detected by LuxR. E. coli encodes a LuxR homologue, SdiA, but it does not encode a LuxI homologue or synthesize any AHL molecule detected by SdiA. However, SdiA of E. coli responds to several AHLs generated by other microbial species. Recently a report indicates that E. coli uses SdiA to monitor indole and AHLs to control biofilms, however, it is not ascertained whether indole itself binds to SdiA. A previous study shows that SdiA can support or inhibit RNA polymerase binding to the promoters and thereby affects transcription of the target genes. Overexpression of SdiA affects expression of a battery of genes, including cell division, motility, chemotaxis, and multidrug efflux pump genes.E. coli has an intact quorum sensing system 2 including nine genes (e.g. luxS, lsrR, lsrK and lsrACDBFG). cAMP-CRP complex stimulates expression of both lsrR and lsr operon which includes IsrACDBFG, while LsrR represses their expression and is located adjacent to but is transcribed divergently from the lsr operon. The system 2 autoinducer named AI-2 is synthesized by LuxS and accumulates extracellularly. Following internalization by the Lsr transporter encoded by the genes in the lsr operon, AI-2 is phosphorylated by LsrK and phospho-AI-2 binds specifically to LsrR and antagonizes it. LsrF and LsrG are required for further processing of phospho-AI-2. It has been recently reported that the mean biofilm thickness and biomass of the lsrR or lsrK mutant are lower than that of the wild type, meanwhile, the global small RNA (sRNA) regulator DsrA and the sRNA cell division inhibitor DicF are induced 2 to 4.4-fold in both lsrR and lsrK mutants.Three quorum sensing circuits of Vibrio harveyi converge to control a same set of genes, in which sRNA species are involved. In E. coli, cAMP-CRP complex stimulates expression of both lsrR and lsr operon by binding to the promoter regions, while LsrR represses their expression. The relationship between QS system 1 and QS system 2 in E. coli, however, remains obscure. To further explore quorum sensing in E. coli, and the relationship between quorum sensing and other signaling pathways, we analyzed the transcription regulation of ydiV expression by SdiA, and the interaction between SdiA and quorum sensing system 2, by employing these biological technologies, such as gene knock out, gel shift and enzyme activity assay, et al. A class of enzymes containing GGDEF domains synthesize the second messenger c-di-GMP in bacterium that is later hydrolyzed by EAL domain proteins. The protein YdiV consists solely of an EAL domain. Here we show that expression of sdiA and ydiV is inhibited by glucose. SdiA binds to ydiV promoter region in a dose-dependent manner, but nonspecifically in the present study, and AI-1 from other species stimulates ydiV expression in an sdiA -dependent manner. Furthermore, we discover that the double sdiA-ydiV mutation but not the single mutations causes a decrease in intracellular cAMP concentration by 2-fold that leads to the inhibition of QS system 2. These results demonstrate that YdiV and cAMP are involved in the interaction between the two QS systems in E. coli, and indicate that signaling pathways which respond to important environmental cues, such as autoinducers and glucose, are linked together for their control in E. coli.