scholarly journals Quorum Sensing-Mediated and Growth Phase-Dependent Regulation of Metabolic Pathways in Hafnia alvei H4

2021 ◽  
Vol 12 ◽  
Author(s):  
Congyang Yan ◽  
Xue Li ◽  
Gongliang Zhang ◽  
Yaolei Zhu ◽  
Jingran Bi ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Cell Density ◽  
Growth Phase ◽  
Metabolic Pathways ◽  
High Cell Density ◽  
Dependent Manner ◽  
High Cell ◽  
Wild Type ◽  
Hafnia Alvei ◽  
Density Dependent

Quorum sensing (QS) is a widespread regulatory mechanism in bacteria used to coordinate target gene expression with cell density. Thus far, little is known about the regulatory relationship between QS and cell density in terms of metabolic pathways in Hafnia alvei H4. In this study, transcriptomics analysis was performed under two conditions to address this question. The comparative transcriptome of H. alvei H4 wild-type at high cell density (OD600 = 1.7) relative to low cell density (OD600 = 0.3) was considered as growth phase-dependent manner (GPDM), and the transcriptome profile of luxI/R deletion mutant (ΔluxIR) compared to the wild-type was considered as QS-mediated regulation. In all, we identified 206 differentially expressed genes (DEGs) mainly presented in chemotaxis, TCA cycle, two-component system, ABC transporters and pyruvate metabolism, co-regulated by the both density-dependent regulation, and the results were validated by qPCR and swimming phenotypic assays. Aside from the co-regulated DEGs, we also found that 59 DEGs, mediated by density-independent QS, function in pentose phosphate and histidine metabolism and that 2084 cell-density-dependent DEGs involved in glycolysis/gluconeogenesis and phenylalanine metabolism were influenced only by GPDM from significantly enriched analysis of transcriptome data. The findings provided new information about the interplay between two density-dependent metabolic regulation, which could assist with the formulation of control strategies for this opportunistic pathogen, especially at high cell density.

scholarly journals Quorum Sensing Controls Biofilm Formation in Vibrio cholerae through Modulation of Cyclic Di-GMP Levels and Repression of vpsT

2008 ◽  
Vol 190 (7) ◽  
pp. 2527-2536 ◽  
Author(s):  
Christopher M. Waters ◽  
Wenyun Lu ◽  
Joshua D. Rabinowitz ◽  
Bonnie L. Bassler
Keyword(s):  
Quorum Sensing ◽  
Vibrio Cholerae ◽  
Cell Density ◽  
Biofilm Formation ◽  
High Cell Density ◽  
High Cell ◽  
Chemical Signaling ◽  
Signaling Systems ◽  
Genes Encoding ◽  
Low Cell Density

ABSTRACT Two chemical signaling systems, quorum sensing (QS) and 3′,5′-cyclic diguanylic acid (c-di-GMP), reciprocally control biofilm formation in Vibrio cholerae. QS is the process by which bacteria communicate via the secretion and detection of autoinducers, and in V. cholerae, QS represses biofilm formation. c-di-GMP is an intracellular second messenger that contains information regarding local environmental conditions, and in V. cholerae, c-di-GMP activates biofilm formation. Here we show that HapR, a major regulator of QS, represses biofilm formation in V. cholerae through two distinct mechanisms. HapR controls the transcription of 14 genes encoding a group of proteins that synthesize and degrade c-di-GMP. The net effect of this transcriptional program is a reduction in cellular c-di-GMP levels at high cell density and, consequently, a decrease in biofilm formation. Increasing the c-di-GMP concentration at high cell density to the level present in the low-cell-density QS state restores biofilm formation, showing that c-di-GMP is epistatic to QS in the control of biofilm formation in V. cholerae. In addition, HapR binds to and directly represses the expression of the biofilm transcriptional activator, vpsT. Together, our results suggest that V. cholerae integrates information about the vicinal bacterial community contained in extracellular QS autoinducers with the intracellular environmental information encoded in c-di-GMP to control biofilm formation.

scholarly journals Contact inhibition of growth of human diploid fibroblasts by immobilized plasma membrane glycoproteins.

1986 ◽  
Vol 103 (2) ◽  
pp. 361-367 ◽  
Author(s):  
R J Wieser ◽  
F Oesch
Keyword(s):  
Plasma Membrane ◽  
Cell Density ◽  
High Cell Density ◽  
Human Fibroblasts ◽  
Dependent Manner ◽  
High Cell ◽  
Membrane Glycoproteins ◽  
Type Iii ◽  
Inhibition Of Growth ◽  
Terminal Galactose

The human embryonic fibroblasts used in this study show pronounced inhibition of growth when reaching a critical cell density. High cell density and growth inhibition has previously been mimicked by the addition of glutaraldehyde-fixed cells or of isolated plasma membranes to sparsely seeded proliferating fibroblasts (Wieser, R. J., R. Heck, and F. Oesch, 1985, Exp. Cell Res., 158:493-499). In this report, we describe the successful solubilization of the growth-inhibiting glycoproteins and their covalent coupling to silicabeads (10 microns), which had been derivatized with 3-isothiocyanatopropyltriethoxysilane. The beads, bearing the plasma membrane proteins, were added to sparsely seeded, actively proliferating fibroblasts, and growth was measured by the determination of cell number or of incorporation of [3H]thymidine into DNA. The growth was inhibited in a concentration-dependent manner, whereby 50% inhibition was achieved with 0.3 micrograms of immobilized protein added to 5 X 10(3) cells. Terminal galactose residues of plasma membrane glycoproteins with N-glycosydically bound carbohydrates were responsible for the inhibition of growth. Dense cultures of human fibroblasts are characterized by an accelerated synthesis of procollagen type III. We have found that this cellular response can also be induced by the addition of immobilized plasma membrane glycoproteins to sparsely seeded cells. These observations support the conclusion that the addition of immobilized plasma membrane glycoproteins to sparsely seeded fibroblasts mimics the situation occurring at high cell density. These results show that cell-cell contacts via plasma membrane glycoproteins carrying terminal galactose residues are important for the regulation of the proliferation of cultured human fibroblasts and presumably of the accelerated synthesis of collagen type III.

scholarly journals The quorum sensing transcription factor AphA directly regulates natural competence in Vibrio cholerae

2019 ◽  
Author(s):  
James R. J. Haycocks ◽  
Gemma Z. L. Warren ◽  
Lucas M. Walker ◽  
Jennifer L. Chlebek ◽  
Triana N. Dalia ◽  
...  
Keyword(s):  
Dna Binding ◽  
Quorum Sensing ◽  
Vibrio Cholerae ◽  
Cell Density ◽  
High Cell Density ◽  
Financial Burden ◽  
Ectopic Expression ◽  
Dna Uptake ◽  
High Cell ◽  
Natural Competence

ABSTRACTMany bacteria use population density to control gene expression via quorum sensing. In Vibrio cholerae, quorum sensing coordinates virulence, biofilm formation, and DNA uptake by natural competence. The transcription factors AphA and HapR, expressed at low- and high-cell density respectively, play a key role. In particular, AphA triggers the entire virulence cascade upon host colonisation. In this work we have mapped genome-wide DNA binding by AphA. We show that AphA is versatile, exhibiting distinct modes of DNA binding and promoter regulation. Unexpectedly, whilst HapR is known to induce natural competence, we demonstrate that AphA also intervenes. Most notably, AphA is a direct repressor of tfoX, the master activator of competence. Hence, production of AphA markedly suppressed DNA uptake; an effect largely circumvented by ectopic expression of tfoX. Our observations suggest dual regulation of competence. At low cell density AphA is a master repressor whilst HapR activates the process at high cell density. Thus, we provide deep mechanistic insight into the role of AphA and highlight how V. cholerae utilises this regulator for diverse purposes.AUTHOR SUMMARYCholera remains a devastating diarrhoeal disease responsible for millions of cases, thousands of deaths, and a $3 billion financial burden every year. Although notorious for causing human disease, the microorganism responsible for cholera is predominantly a resident of aquatic environments. Here, the organism survives in densely packed communities on the surfaces of crustaceans. Remarkably, in this situation, the microbe can feast on neighbouring cells and acquire their DNA. This provides a useful food source and an opportunity to obtain new genetic information. In this paper, we have investigated how acquisition of DNA from the local environment is regulated. We show that a “switch” within the microbial cell, known to activate disease processes in the human host, also controls DNA uptake. Our results explain why DNA scavenging only occurs in suitable environments and illustrates how interactions between common regulatory switches affords precise control of microbial behaviours.

Quorum sensing regulates the transcription of lateral flagellar genes in Vibrio parahaemolyticus

2019 ◽  
Vol 14 (12) ◽  
pp. 1043-1053 ◽  
Author(s):  
Renfei Lu ◽  
Hao Tang ◽  
Yue Qiu ◽  
Wenhui Yang ◽  
Huiying Yang ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Cell Density ◽  
Vibrio Parahaemolyticus ◽  
High Cell Density ◽  
High Cell ◽  
Regulatory Effect ◽  
Swarming Motility ◽  
Dnase I Footprinting ◽  
Regulation Mechanisms ◽  
Low Cell Density

Aim: Investigation of the lateral flagellar (Laf) genes transcription by the quorum sensing (QS) regulators AphA and OpaR in Vibrio parahaemolyticus. Materials & methods: Regulation mechanisms were assessed by combined utilization of swarming motility assay, qPCR, LacZ fusion, EMSA and DNase I footprinting. Results: AphA and OpaR oppositely regulate swarming motility and Laf genes. At high cell density, OpaR bound to the regulatory regions of motY-lafK-fliEFGHIJ, fliMNPQR-flhBA, fliDSTKLA-motAB and lafA to repress their transcription. At low cell density, AphA indirectly activated their transcription. Conclusion: OpaR repression of swarming motility was via its direct repression of Laf genes, while AphA exerted its regulatory effect on swarming motility through unknown regulator(s).

scholarly journals The Fur-Iron Complex Modulates Expression of the Quorum-Sensing Master Regulator, SmcR, To Control Expression of Virulence Factors in Vibrio vulnificus

2013 ◽  
Vol 81 (8) ◽  
pp. 2888-2898 ◽  
Author(s):  
In Hwang Kim ◽  
Yancheng Wen ◽  
Jee-Soo Son ◽  
Kyu-Ho Lee ◽  
Kun-Soo Kim
Keyword(s):  
Quorum Sensing ◽  
Cell Density ◽  
Virulence Factors ◽  
Vibrio Vulnificus ◽  
High Cell Density ◽  
Iron Complex ◽  
High Cell ◽  
Mobility Shift ◽  
Master Regulator ◽  
Content Type

ABSTRACTThe genevvpE, encoding the virulence factor elastase, is a member of the quorum-sensing regulon inVibrio vulnificusand displays enhanced expression at high cell density. We observed that this gene was repressed under iron-rich conditions and that the repression was due to a Fur (ferricuptakeregulator)-dependent repression ofsmcR, a gene encoding a quorum-sensing master regulator with similarity toluxRinVibrio harveyi. A gel mobility shift assay and a footprinting experiment demonstrated that the Fur-iron complex binds directly to two regions upstream ofsmcR(−82 to −36 and −2 to +27, with respect to the transcription start site) with differing affinities. However, binding of the Fur-iron complex is reversible enough to allow expression ofsmcRto be induced by quorum sensing at high cell density under iron-rich conditions. Under iron-limiting conditions, Fur fails to bind either region and the expression ofsmcRis regulated solely by quorum sensing. These results suggest that two biologically important environmental signals, iron and quorum sensing, converge to direct the expression ofsmcR, which then coordinates the expression of virulence factors.

scholarly journals Ethanolamine regulates CqsR quorum-sensing signaling inVibrio cholerae

2019 ◽  
Author(s):  
Samit Watve ◽  
Kelsey Barrasso ◽  
Sarah A. Jung ◽  
Kristen J. Davis ◽  
Lisa A. Hawver ◽  
...  
Keyword(s):  
Gene Expression ◽  
Quorum Sensing ◽  
Vibrio Cholerae ◽  
Cell Density ◽  
High Cell Density ◽  
Chemical Signals ◽  
Communication Process ◽  
Control Group ◽  
Dual Function ◽  
High Cell

ABSTRACTThe pathogen that causes cholera,Vibrio cholerae, uses the cell-cell communication process known as quorum sensing (QS) to regulate virulence factor production and biofilm formation in response to changes in population density and complexity. QS is mediated through the detection of extracellular chemical signals called autoinducers. Four histidine kinases, LuxPQ, CqsS, CqsR and VpsS, have been identified as receptors to activate the key QS regulator LuxO at low cell density. At high cell density, detection of autoinducers by these receptors leads to deactivation of LuxO, resulting in population-wide gene expression changes. While the cognate autoinducers that regulate the activity of CqsS and LuxQ are known, the signals that regulate CqsR have not been determined. Here we show that the common metabolite ethanolamine specifically interacts with the ligand-binding CACHE domain of CqsRin vitroand induces the high cell-density QS response through CqsR kinase inhibition inV. choleraecells. We also identified residues in the CqsR CACHE domain important for ethanolamine detection and signal transduction. Moreover, mutations disrupting endogenous ethanolamine production inV. choleraedelay the onset of, but do not abolish, the high cell-density QS gene expression. Finally, we demonstrate that modulation of CqsR QS response by ethanolamine occurs inside animal hosts. Our findings suggest thatV. choleraeuses CqsR as a dual-function receptor to integrate information from the self-made signals as well as exogenous ethanolamine as an environmental cue to modulate QS response.IMPORTANCEMany bacteria use quorum sensing to regulate cellular processes that are important for their survival and adaptation to different environments. Quorum sensing usually depends on the detection on chemical signals called autoinducers made endogenously by the bacteria. We show here ethanolamine, a common metabolite made by various bacteria and eukaryotes, can modulate the activity of one of the quorum-sensing receptors inVibrio cholerae, the etiological agent of the disease cholera. Our results raise the possibility thatV. choleraeor other quorum-sensing bacteria can combine environmental sensing and quorum sensing to control group behaviors.

scholarly journals Reduced Levels of ATF-2 Predispose Mice to Mammary Tumors

2006 ◽  
Vol 27 (5) ◽  
pp. 1730-1744 ◽  
Author(s):  
Toshio Maekawa ◽  
Toshie Shinagawa ◽  
Yuji Sano ◽  
Takahiko Sakuma ◽  
Shintaro Nomura ◽  
...  
Keyword(s):  
Cell Density ◽  
Target Genes ◽  
High Cell Density ◽  
Critical Role ◽  
Susceptibility Gene ◽  
Mammary Tumors ◽  
Mrna Levels ◽  
High Cell ◽  
Wild Type ◽  
Induced Apoptosis

ABSTRACT Transcription factor ATF-2 is a nuclear target of stress-activated protein kinases, such as p38, which are activated by various extracellular stresses, including UV light. Here, we show that ATF-2 plays a critical role in hypoxia- and high-cell-density-induced apoptosis and the development of mammary tumors. Compared to wild-type cells, Atf-2 −/− mouse embryonic fibroblasts (MEFs) were more resistant to hypoxia- and anisomycin-induced apoptosis but remained equally susceptible to other stresses, including UV. Atf-2 −/− and Atf-2 +/− MEFs could not express a group of genes, such as Gadd45α, whose overexpression can induce apoptosis, in response to hypoxia. Atf-2 −/− MEFs also had a higher saturation density than wild-type cells and expressed lower levels of Maspin, the breast cancer tumor suppressor, which is also known to enhance cellular sensitivity to apoptotic stimuli. Atf-2 −/− MEFs underwent a lower degree of apoptosis at high cell density than wild-type cells. Atf-2 +/− mice were highly prone to mammary tumors that expressed reduced levels of Gadd45α and Maspin. The ATF-2 mRNA levels in human breast cancers were lower than those in normal breast tissue. Thus, ATF-2 acts as a tumor susceptibility gene of mammary tumors, at least partly, by activating a group of target genes, including Maspin and Gadd45α.

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