scholarly journals Vibrio fischeri LuxS and AinS: Comparative Study of Two Signal Synthases

2004 ◽  
Vol 186 (12) ◽  
pp. 3873-3881 ◽  
Author(s):  
Claudia Lupp ◽  
Edward G. Ruby
Keyword(s):  
Gene Expression ◽  
Vibrio Fischeri ◽  
Fold Increase ◽  
Homoserine Lactone ◽  
Autoinducer 2 ◽  
Light Production ◽  
Two Systems ◽  
Cell Densities ◽  
Quantitative Contribution ◽  
The Impact

ABSTRACT Vibrio fischeri possesses two acyl-homoserine lactone quorum-sensing systems, ain and lux, both of which are involved in the regulation of luminescence gene expression and are required for persistent colonization of the squid host, Euprymna scolopes. We have previously demonstrated that the ain system induces luminescence at cell densities that precede lux system activation. Our data suggested that the ain system both relieves repression and initially induces the lux system, thereby achieving sequential induction of gene expression by these two systems. Analysis of the V. fischeri genome revealed the presence of a putative third system based on the enzyme LuxS, which catalyzes the synthesis of the Vibrio harveyi autoinducer 2 (AI-2). In this study, we investigated the impact of V. fischeri LuxS on luminescence and colonization competence in comparison to that of the ain system. Similar to the ain system, inactivation of the AI-2 system decreased light production in culture, but not in the squid host. However, while an ainS mutant produces no detectable light in culture, a luxS mutant expressed approximately 70% of wild-type luminescence levels. A mutation in luxS alone did not compromise symbiotic competence of V. fischeri; however, levels of colonization of an ainS luxS double mutant were reduced to 50% of the already diminished level of ainS mutant colonization, suggesting that these two systems regulate colonization gene expression synergistically through a common pathway. Introduction of a luxO mutation into the luxS and ainS luxS background could relieve both luminescence and colonization defects, consistent with a model in which LuxS, like AinS, regulates gene expression through LuxO. Furthermore, while luxS transcription appeared to be constitutive and the AI-2 signal concentration did not change dramatically, our data suggest that ainS transcription is autoregulated, resulting in an over 2,000-fold increase in signal concentration as culture density increased. Taken together, these data indicate that V. fischeri LuxS affects both luminescence regulation and colonization competence; however, its quantitative contribution is small when compared to that of the AinS signal.

scholarly journals Novel Reporter for Identification of Interference with Acyl Homoserine Lactone and Autoinducer-2 Quorum Sensing

2014 ◽  
Vol 81 (4) ◽  
pp. 1477-1489 ◽  
Author(s):  
Nancy Weiland-Bräuer ◽  
Nicole Pinnow ◽  
Ruth A. Schmitz
Keyword(s):  
Quorum Sensing ◽  
Vibrio Fischeri ◽  
Quorum Quenching ◽  
Homoserine Lactone ◽  
Signal Molecules ◽  
Lethal Gene ◽  
Reporter Strain ◽  
Content Type ◽  
E Coli ◽  
Autoinducer 2

ABSTRACTTwo reporter strains were established to identify novel biomolecules interfering with bacterial communication (quorum sensing [QS]). The basic design of theseEscherichia coli-based systems comprises a gene encoding a lethal protein fused to promoters induced in the presence of QS signal molecules. Consequently, theseE. colistrains are unable to grow in the presence of the respective QS signal molecules unless a nontoxic QS-interfering compound is present. The first reporter strain designed to detect autoinducer-2 (AI-2)-interfering activities (AI2-QQ.1) contained theE. coliccdBlethal gene under the control of theE. colilsrApromoter. The second reporter strain (AI1-QQ.1) contained theVibrio fischeriluxIpromoter fused to theccdBgene to detect interference with acyl-homoserine lactones. Bacteria isolated from the surfaces of several marine eukarya were screened for quorum-quenching (QQ) activities using the established reporter systems AI1-QQ.1 and AI2-QQ.1. Out of 34 isolates, two interfered with acylated homoserine lactone (AHL) signaling, five interfered with AI-2 QS signaling, and 10 were demonstrated to interfere with both signal molecules. Open reading frames (ORFs) conferring QQ activity were identified for three selected isolates (Photobacteriumsp.,Pseudoalteromonassp., andVibrio parahaemolyticus). Evaluation of the respective heterologously expressed and purified QQ proteins confirmed their ability to interfere with the AHL and AI-2 signaling processes.

scholarly journals Critical symbiont signals drive both local and systemic changes in diel and developmental host gene expression

2019 ◽  
Vol 116 (16) ◽  
pp. 7990-7999 ◽  
Author(s):  
Silvia Moriano-Gutierrez ◽  
Eric J. Koch ◽  
Hailey Bussan ◽  
Kymberleigh Romano ◽  
Mahdi Belcaid ◽  
...  
Keyword(s):  
Gene Expression ◽  
Visual Cues ◽  
Vibrio Fischeri ◽  
Single Mutation ◽  
Light Organ ◽  
Euprymna Scolopes ◽  
Transcriptional Responses ◽  
Transcriptional Signature ◽  
The Impact ◽  
Organ Colonization

The colonization of an animal’s tissues by its microbial partners creates networks of communication across the host’s body. We used the natural binary light-organ symbiosis between the squidEuprymna scolopesand its luminous bacterial partner,Vibrio fischeri, to define the impact of colonization on transcriptomic networks in the host. A night-active predator,E. scolopescoordinates the bioluminescence of its symbiont with visual cues from the environment to camouflage against moon and starlight. Like mammals, this symbiosis has a complex developmental program and a strong day/night rhythm. We determined how symbiont colonization impacted gene expression in the light organ itself, as well as in two anatomically remote organs: the eye and gill. While the overall transcriptional signature of light organ and gill were more alike, the impact of symbiosis was most pronounced and similar in light organ and eye, both in juvenile and adult animals. Furthermore, the presence of a symbiosis drove daily rhythms of transcription within all three organs. Finally, a single mutation inV. fischeri—specifically, deletion of theluxoperon, which abrogates symbiont luminescence—reduced the symbiosis-dependent transcriptome of the light organ by two-thirds. In addition, while the gills responded similarly to light-organ colonization by either the wild-type or mutant, luminescence was required for all of the colonization-associated transcriptional responses in the juvenile eye. This study defines not only the impact of symbiont colonization on the coordination of animal transcriptomes, but also provides insight into how such changes might impact the behavior and ecology of the host.

Abstract 1330: Divergent Control of the Mitochondrial Death Gene BNIP3 by Opposing Actions of the Cellular Factors Nuclear Factor kappaB and E2F-1 in Ventricular Myocytes.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
James Shaw ◽  
Natalia Yurkova ◽  
Kelly Regula ◽  
Tong Zhang ◽  
Floribeth Aguilar ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Dna Binding ◽  
Gene Transcription ◽  
Ventricular Myocytes ◽  
Fold Increase ◽  
Genetic Ablation ◽  
The Impact ◽  
Chip Analysis ◽  
In Cells

The hypoxia-inducible death factor Bnip3 is known to provoke mitochondrial perturbations and cell death of ventricular myocytes. The transcriptional control processes that govern Bnip3 gene expression under basal and inducible conditions remain cryptic. Sequence analysis of the Bnip3 promoter revealed the presence of distinct but overlapping DNA binding elements for the cell cycle factor E2F-1 and cellular factor NF-κB. Previously, we reported a survival role for NF-κB in ventricular myocytes. As a step toward elucidating the regulation of Bnip3 gene expression in ventricular myocytes, we tested the impact of E2F-1 and NF-κB on basal and inducible expression of Bnip3. A 2.0 fold increase in Bnip3 gene transcription was observed in cells expression wild type E2F-1 but not in cells expressing an E2F-1 mutant defective for DNA binding. Interestingly, basal Bnip3 gene transcription was increased by 2.5 fold in myocytes rendered defective for NF-κB activation with a non-phosphorylatable form of IκBα. Importantly, genetic ablation of E2F-1 inhibited basal and inducible Bnip3 transcription in NF-κB defective cells. Expression of the p65 subunit of NF-κB in NF-κB defective cells inhibited E2F-1 mediated Bnip3 transcription. Western blot analysis of cardiac cell lysate revealed that p65 NF-κB immunoprecipitated with E2F-1. ChIP analysis of the Bnip3 promoter indicated that the p65 NF-κB bound DNA under normoxic conditions. During hypoxia E2F-1 activity increased where as p65 NF-κB protein levels were decreased. ChIP analysis revealed increased binding of E2F-1 to the Bnip3 promoter during hypoxia which coincided with a 3.5 fold increase in Bnip3 gene transcription. IKKβ mediated activation of NF-κB activation abrogated hypoxia-induced E2F-1 binding to the Bnip3 promoter and Bnip3 gene transcription. To our knowledge our data provide the first direct evidence that a novel relationship exists between p65 NF-κB and E2F-1 for basal and hypoxia-inducible regulation of the Bnip3 promoter. Furthermore, our data highlight a novel survival pathway by which NF-κB averts hypoxia - induced cell death by antagonizing the E2F-1 dependent transcription of Bnip3 in ventricular myocytes.

Elevated Expression of GPR34 in Mucosa-Associated Lymphoid Tissue (MALT) Lymphoma and Its Association with Increased Cell Growth, Erk Activation, and AP-1 and CRE-Mediated Transcription.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3927-3927
Author(s):  
Anne J Novak ◽  
Takashi Akasaka ◽  
Michelle Manske ◽  
Tammy Price-Troska ◽  
Mamta Gupta ◽  
...  
Keyword(s):  
Gene Expression ◽  
B Cells ◽  
Cell Growth ◽  
Vector Control ◽  
Mrna Expression ◽  
Malt Lymphoma ◽  
Fold Increase ◽  
Luciferase Reporter ◽  
Elevated Expression ◽  
The Impact

Abstract Abstract 3927 Poster Board III-863 In previous studies we characterized the t(X;14)(p11.4;q32) translocation in a patient with MALT lymphoma and found that GPR34, an orphan G-protein coupled receptor (GPCR), was highly expressed due to its juxtaposition to the IGHSA2 switch region. As part of a larger MALT gene expression-profiling project, we have now acquired gene expression analysis on the patient carrying the t(X;14)(p11;q32) translocation and have confirmed overexpression of GPR34. We then measured GPR34 mRNA expression in a panel of MALT lymphomas (n=17) and found that GPR34 was expressed at levels higher than that seen in normal B cells (mean, 11.3 fold; median, 5.5; range, 1.4-64 fold). When analyzed separately, 70% (12/17) had an expression level greater than 3-fold over normal B cells. Of note, in a gastric MALT lymphoma specimen, we found a 64 fold increase in GPR34 mRNA expression. FISH studies performed on this specimen showed an extra intact GPR34 signal but no translocation involving IGH or GPR34, suggesting that other mechanisms, including gene dosage effect, can upregulate GPR34. Elevated expression of GPR34 mRNA was also detected in other histologic types of NHL, but not to the extent seen in MALT lymphoma. Taken together, these data suggest that GPR34 is commonly overexpressed in MALT lymphoma and that deregulation of GPR34 expression can occur independent of a t(X;14)(p11.4;q32) translocation. The receptor encoded by GPR34 is most similar to the PY2 receptor subfamily of GPCR and GPR34 mRNA transcripts are abundant in mast cells while lower levels were detected in other immune cells including B cells. Signals from GPR34 have been briefly described and the results to date suggest that overexpression of GPR34 results in an accumulation of inositol phosphates. To further characterize the impact of GPR34 overexpression on cell signaling, HeLa cells were transduced with a retroviral expression plasmid (pBMN-GFP) that expresses GPR34 and GFP. GFP expressing cells were isolated and overexpression of GPR34 mRNA was confirmed by PCR and GPR34 protein expression was detected by flow cytometry. When normalized to the isotype control, pBMN-GPR34 cells expressed 17-fold more GPR34 on their cell surface compared to the pBMN-vector control cells. To determine which signaling pathways were affected by GPR34 overexpression, pBMN-GPR34 or pBMN-vector control cells were transfected with an AP-1, CRE, NF-κB, E2F, SRE, NFAT, or ISRE- luciferase reporter plasmid. Upon normalization with renilla, pBMN-GPR34 expressing cells had increased luciferase activity (n=3) driven by AP-1 (5.35-fold), CRE (4.7), NF-κB (2.8-fold), and E2F (2.13) when compared to pBMN-vector control cells. ISRE, NFAT, and SRE mediated luciferase expression was similar in the GPR34 and control cells. AP-1 and CRE have been implicated in a large variety of cellular processes, including transformation, and both AP-1 and CRE activity is induced upon activation of MAP kinases. To determine if MAPK activity was also upregulated in GPR34 expressing cells, we analyzed the phosphorylation status of Erk1/2 in pBMN-GPR34 cells by western blot and found that Erk1/2 was constitutively phosphorylated in GRP34 expressing cells (1.8 fold increase) compared to vector control cells. Increased phosphorylation of PKC-α/β was also detected in pBMN-GPR34 cells (3.5 fold increase compared to control cells). To determine the biologic impact of GRP34 overexpression on cell growth, the proliferation rates of pBMN-control and pBMN-GPR34 cells were compared and it was found that proliferation of GPR34 expressing cells was 2.2 times higher than that seen in control cells. Because the MAPK kinase pathway was found to be active in the pBMN-GPR34 cells, we tested the effect of the MEK inhibitor PD98059 on proliferation and saw a dose dependent decrease in proliferation of GPR34 expressing cells. These results suggest that GPR34-mediated proliferation is Erk-dependent. In summary, these data suggest that deregulation of GPR34 is commonly found in MALT lymphoma and that overexpression of GPR34 results in activation of Erk1/2, phosphorylation of PKC, and results is AP-1 and CRE mediated transcription. Additionally, our data suggest that overexpression of GPR34 results in increased cell growth that is MAPK-dependent. Taken together, this studies indicate that overexpression of a GPCR, GPR34, may be a novel mechanism by which MALT, lymphoma, and potentially other subtypes of NHL, develop. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Gene Expression in Amnion-Derived Cells Cultured on Recombinant Laminin 332—A Preliminary Study

2021 ◽  
Vol 8 ◽  
Author(s):  
Katarzyna Skowron-Kandzia ◽  
Marcin Tomsia ◽  
Halina Koryciak-Komarska ◽  
Danuta Plewka ◽  
Patrycja Wieczorek ◽  
...  
Keyword(s):  
Gene Expression ◽  
Ex Vivo ◽  
Self Regulation ◽  
Fold Increase ◽  
Differentiation Markers ◽  
Differentiated Cells ◽  
Immunomodulatory Properties ◽  
The Impact ◽  
Laminin 332 ◽  
Amniotic Cells

Human amniotic cells (hAC) exhibit characteristics of undifferentiated cells and immunomodulatory properties. Recognition of the relationship between amniotic cells and components of the extracellular matrix is an important condition for their ex vivo preparation and further successful clinical application in regenerative medicine and transplantology. Laminin 332 (LN-332), as a natural component of the basement membrane of amniotic epithelial cells and a ligand for integrin receptors, may strongly influence the phenotype and fate of amniotic cells. We investigated the impact of recombinant LN-332 on hAC viability and expression of markers for pluripotency, early differentiation, adhesion, and immunomodulatory properties. During 14 days of culture, hAC were quantified and qualified by light microscopy, immunohistochemistry, immunocytochemistry, and flow cytometry. Gene expression was assessed with real-time polymerase chain reaction (RT-PCR) arrays and compared with differentiated cells originated from the three germ layers. LN-332 caused an over 2-fold increase in the total number of hAC, accompanied by a 75% reduction of SSEA-4-positive cells and an increase in HLA-ABC-positive cells. In particular, we observed that the presence of laminin 332 in the medium of a short-time culture modifies the effect of culture duration on hAC, enhancing time-dependent inhibition of expression of certain genes, including pluripotency and differentiation markers, laminin 332 subunits (which may be part of self-regulation of LN-332 synthesis by amniotic cells), and integrins. The changes observed in hAC were more distinct with respect to differentiated mesenchymal cells, resulting in more comparable phenotypes than those represented by differentiated endo- and ectodermal cells. We concluded that laminin 332 present in the culture medium influences to a certain extent proliferation, adhesion, and differentiation of amniotic cells in culture.

scholarly journals Probing the Impact of Ligand Binding on the Acyl-Homoserine Lactone-Hindered Transcription Factor EsaR of Pantoea stewartii subsp. stewartii

2011 ◽  
Vol 193 (22) ◽  
pp. 6315-6322 ◽  
Author(s):  
Daniel J. Schu ◽  
Revathy Ramachandran ◽  
Jared S. Geissinger ◽  
Ann M. Stevens
Keyword(s):  
Conformational Changes ◽  
Homoserine Lactone ◽  
Biologically Active ◽  
Acyl Homoserine Lactone ◽  
Content Type ◽  
Pantoea Stewartii ◽  
Cell Densities ◽  
The Impact

The quorum-sensing regulator EsaR fromPantoea stewartiisubsp.stewartiiis a LuxR homologue that is inactivated by acyl-homoserine lactone (AHL). In the corn pathogenP. stewartii, production of exopolysaccharide (EPS) is repressed by EsaR at low cell densities. However, at high cell densities when high concentrations of its cognate AHL signal are present, EsaR is inactivated and derepression of EPS production occurs. Thus, EsaR responds to AHL in a manner opposite to that of most LuxR family members. Depending on the position of its binding site within target promoters, EsaR serves as either a repressor or activator in the absence rather than in the presence of its AHL ligand. The effect of AHL on LuxR homologues has been difficult to studyin vitrobecause AHL is required for purification and stability. EsaR, however, can be purified without AHL enabling anin vitroanalysis of the response of the protein to ligand. Western immunoblots and pulse-chase experiments demonstrated that EsaR is stablein vivoin the absence or presence of AHL. Limitedin vitroproteolytic digestions of a biologically active His-MBP tagged version of EsaR highlighted intradomain and interdomain conformational changes that occur in the protein in response to AHL. Gel filtration chromatography of the full-length fusion protein and cross-linking of the N-terminal domain both suggest that this conformational change does not impact the multimeric state of the protein. These findings provide greater insight into the diverse mechanisms for AHL responsiveness found within the LuxR family.

scholarly journals GacA Regulates Symbiotic Colonization Traits ofVibrio fischeri and Facilitates a Beneficial Association withan AnimalHost

2003 ◽  
Vol 185 (24) ◽  
pp. 7202-7212 ◽  
Author(s):  
Cheryl A. Whistler ◽  
Edward G. Ruby
Keyword(s):  
Vibrio Fischeri ◽  
Growth Yield ◽  
Homoserine Lactone ◽  
Symbiotic Association ◽  
Wild Type ◽  
Population Densities ◽  
Light Production ◽  
Light Organs ◽  
Type Population

ABSTRACT The GacS/GacA two-component system regulates the expression of bacterial traits during host association. Although the importance of GacS/GacA as a regulator of virulence is well established, its role in benign associations is not clear, as mutations in either the gacS or gacA gene have little impact on the success of colonization in nonpathogenic associations studied thus far. Using as a model the symbiotic association of the bioluminescent marine bacterium Vibrio fischeri with its animal host, the Hawaiian bobtail squid, Euprymna scolopes, we investigated the role of GacA in this beneficial animal-microbe interaction. When grown in culture, gacA mutants were defective in several traits important for symbiosis, including luminescence, growth in defined media, growth yield, siderophore activity, and motility. However, gacA mutants were not deficient in production of acylated homoserine lactone signals or catalase activity. The ability of the gacA mutants to initiate squid colonization was impaired but not abolished, and they reached lower-than-wild-type population densities within the host light organ. In contrast to their dark phenotype in culture, gacA mutants that reached population densities above the luminescence detection limit had normal levels of luminescence per bacterial cell in squid light organs, indicating that GacA is not required for light production within the host. The gacA mutants were impaired at competitive colonization and could only successfully cocolonize squid light organs when present in the seawater at higher inoculum densities than wild-type bacteria. Although severely impaired during colonization initiation, gacA mutants were not displaced by the wild-type strain in light organs that were colonized with both strains. This study establishes the role of GacA as a regulator of a beneficial animal-microbe association and indicates that GacA regulates utilization of growth substrates as well as other colonization traits.

scholarly journals Epigenetic regulation of human buccal mucosa mitochondrial superoxide dismutase gene expression by diet

2008 ◽  
Vol 101 (5) ◽  
pp. 743-749 ◽  
Author(s):  
Roman Thaler ◽  
Heidrun Karlic ◽  
Petra Rust ◽  
Alexander G. Haslberger
Keyword(s):  
Gene Expression ◽  
Superoxide Dismutase ◽  
Epigenetic Regulation ◽  
Promoter Methylation ◽  
Fold Increase ◽  
Mitochondrial Superoxide ◽  
Buccal Swabs ◽  
The Impact ◽  
Mitochondrial Superoxide Dismutase ◽  
Mnsod Gene

The impact of nutrition on the epigenetic machinery has increasingly attracted interest. The aim of the present study was to demonstrate the effects of various diets on methylation and gene expression. The antioxidative enzyme mitochondrial superoxide dismutase (MnSOD) was chosen as the model system because epigenetic regulation has been previously shown in cell lines for this gene. Promoter methylation and gene expression of MnSOD in buccal swabs from three sample groups were analysed. The three groups included: (1) forty vegetarians (aged 20–30 years); (2) age-matched omnivores; (3) elderly omnivores (aged>85 years). A 3-fold increase in the expression of the MnSOD gene was associated with decreased CpG methylation of the analysed promoter region in the vegetarian group compared with the age-matched omnivores group. Expression and promoter methylation of the MnSOD gene in elderly omnivores showed no significant differences compared with younger omnivores. In accordance with previous findings in various tissues, DNA global methylation was found to be significantly higher (30 %) in buccal swabs of younger subjects (independent of the diet), than in those of elderly omnivores. In the control experiment which was designed to verify the findings of the human buccal swab studies, the Caco-2 cell line was treated with zebularine. Results of the control study showed a 6-fold increase of MnSOD expression, an approximately 40 % decreased methylation of specified CpG in the MnSOD promoter and a 50 % reduction of global DNA methylation. These results indicate that diet affects the epigenetic regulation of human MnSOD.

scholarly journals A sustained small increase in NOD1 expression promotes ligand-independent oncogenic activity

2019 ◽  
Author(s):  
Leah M. Rommereim ◽  
Ajay Suresh Akhade ◽  
Bhaskar Dutta ◽  
Carolyn Hutcheon ◽  
Nicolas W. Lounsbury ◽  
...  
Keyword(s):  
Gene Expression ◽  
Poor Prognosis ◽  
Protein Concentration ◽  
Complex Disease ◽  
Fold Increase ◽  
Cell State ◽  
Persistent Inflammation ◽  
Small Change ◽  
Genetically Determined ◽  
The Impact

AbstractSmall genetically-determined differences in transcription (eQTLs) are implicated in complex disease but the mechanisms by which small changes in gene expression impact complex disease are unknown. Here we show that a persistent small increase in expression of the innate sensor NOD1 precipitates large cancer-promoting changes in cell state. A ~1.2-1.4 fold increase in NOD1 protein concentration by loss of miR-15b/16 regulation sensitizes cells to ligand-induced inflammation, with an additional slight increase leading to ligand-independent NOD1 activation that is linked to poor prognosis in gastric cancer. Our data show that tight expression regulation of NOD1 prevents this sensor from exceeding a physiological switching checkpoint that promotes persistent inflammation and oncogene expression and reveal the impact of a single small quantitative change in cell state on cancer.One Sentence SummaryA small change in NOD1 expression has a large cancer-promoting impact on cell state.

scholarly journals Transcriptome Analysis of the Vibrio fischeri LuxR-LuxI Regulon

2007 ◽  
Vol 189 (22) ◽  
pp. 8387-8391 ◽  
Author(s):  
Luis Caetano M. Antunes ◽  
Amy L. Schaefer ◽  
Rosana B. R. Ferreira ◽  
Nan Qin ◽  
Ann M. Stevens ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Transcriptome Analysis ◽  
Vibrio Fischeri ◽  
Transcriptional Regulator ◽  
Homoserine Lactone ◽  
Light Production ◽  
Number Of Genes

ABSTRACT The Vibrio fischeri quorum-sensing signal N-3-oxohexanoyl-l-homoserine lactone (3OC6-HSL) activates expression of the seven-gene luminescence operon. We used microarrays to unveil 18 additional 3OC6-HSL-controlled genes, 3 of which had been identified by other means previously. We show most of these genes are regulated by the 3OC6-HSL-responsive transcriptional regulator LuxR directly. This demonstrates that V. fischeri quorum sensing regulates a substantial number of genes other than those involved in light production.

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