scholarly journals Cyclic di-GMP Increases Catalase Production and Hydrogen Peroxide Tolerance in Vibrio cholerae

2019 ◽  
Vol 85 (18) ◽  
Author(s):  
Nicolas L. Fernandez ◽  
Christopher M. Waters
Keyword(s):  
Vibrio Cholerae ◽  
Catalase Activity ◽  
Biofilm Formation ◽  
Salt Water ◽  
Bacterial Pathogen ◽  
Second Messenger ◽  
Signaling Network ◽  
Dependent Manner ◽  
Environmental Persistence ◽  
Content Type

ABSTRACT Vibrio cholerae is a Gram-negative bacterial pathogen that causes the disease cholera, which affects nearly 1 million people each year. In between outbreaks, V. cholerae resides in fresh and salt water environments, where it is able to persist through changes in temperature, oxygen, and salinity. One key characteristic that promotes environmental persistence of V. cholerae is the ability to form multicellular communities, called biofilms, that often adhere to biotic and abiotic sources. Biofilm formation in V. cholerae is positively regulated by the dinucleotide second messenger cyclic dimeric GMP (c-di-GMP). While most research on the c-di-GMP regulon has focused on biofilm formation or motility, we hypothesized that the c-di-GMP signaling network encompassed a larger set of effector functions than reported. We found that high intracellular c-di-GMP increased catalase activity ∼4-fold relative to strains with unaltered c-di-GMP. Genetic studies demonstrated that c-di-GMP mediated catalase activity was due to increased expression of the catalase-encoding gene katB. Moreover, c-di-GMP mediated regulation of catalase activity and katB expression required the c-di-GMP dependent transcription factors VpsT and VpsR. Lastly, we found that high c-di-GMP increased survival after H2O2 challenge in a katB-, vpsR-, and vpsT-dependent manner. Our results indicate that antioxidant production is regulated by c-di-GMP uncovering a new node in the growing VpsT and VpsR c-di-GMP signaling network of V. cholerae. IMPORTANCE As a result of infection with V. cholerae, patients become dehydrated, leading to death if not properly treated. The aquatic environment is the natural reservoir for V. cholerae, where it can survive alterations in temperature, salinity, and oxygen. The second messenger molecule c-di-GMP is an important signal regulating host and aquatic environmental persistence because it controls whether V. cholerae will form a biofilm or disperse through flagellar motility. In this work, we demonstrate another function of c-di-GMP in V. cholerae biology: promoting tolerance to the reactive oxygen species H2O2 through the differential regulation of catalase expression. Our results suggest a mechanism where c-di-GMP simultaneously controls biofilm formation and antioxidant production, which could promote persistence in human and marine environments.

scholarly journals Cyclic di-GMP Increases Catalase Production and Hydrogen Peroxide Tolerance inVibrio cholerae

2019 ◽  
Author(s):  
Nicolas L. Fernandez ◽  
Christopher M. Waters
Keyword(s):  
Catalase Activity ◽  
Biofilm Formation ◽  
Salt Water ◽  
Bacterial Pathogen ◽  
Second Messenger ◽  
Signaling Network ◽  
Guanosine Monophosphate ◽  
Dependent Manner ◽  
Flagellar Motility ◽  
Environmental Persistence

AbstractVibrio choleraeis a Gram-negative bacterial pathogen that causes the disease cholera, which affects nearly 1 million people each year. In between outbreaks,V. choleraeresides in fresh and salt water environments where it is able to persist through changes in temperature, oxygen, and salinity. One key characteristic that promotes environmental persistence ofV. choleraeis the ability to form multicellular communities, called biofilms, that often adhere to biotic and abiotic sources. Biofilm formation inV. choleraeis positively regulated by the dinucleotide second messenger cyclic dimeric guanosine monophosphate (c-di-GMP). While most research on the c-di-GMP regulon has focused on biofilm formation or motility, we hypothesized the c-di-GMP signaling network encompassed a larger set of effector functions than reported. We found that high intracellular c-di-GMP increased catalase activity approximately 4-fold relative to strains with unaltered c-di-GMP. Genetic studies demonstrated that c-di-GMP mediated catalase activity was due to increased expression of the catalase encoding genekatB. Moreover, c-di-GMP mediated regulation of catalase activity andkatBexpression required the c-di-GMP dependent transcription factors VpsT and VpsR. Lastly, we found that high c-di-GMP increased survival after H2O2challenge in akatB, vpsR, andvpsTdependent manner. Our results indicate antioxidant production is regulated by c-di-GMP inV. choleraeuncovering a new node in the growing VpsT and VpsR c-di-GMP signaling network.ImportanceAs a result of infection withV. cholerae, patients become dehydrated leading to death if not properly treated. The marine environment is the natural reservoir forV. choleraewhere it can survive alterations in temperature, salinity, and oxygen. The second messenger molecule c-di-GMP is an important signal regulating host and marine environmental persistence because it controls whetherV. choleraewill form a biofilm or disperse through flagellar motility. In this work, we demonstrate another function of c-di-GMP inV. choleraebiology: promoting tolerance to the reactive oxygen species H2O2through differential regulation of catalase expression. Our results suggest a mechanism where c-di-GMP simultaneously controls biofilm formation and antioxidant production, which could promote persistence in human and marine environments.

scholarly journals A Conserved Regulatory Circuit Controls Large Adhesins in Vibrio cholerae

mBio ◽  
2019 ◽  
Vol 10 (6) ◽  
Author(s):  
Giordan Kitts ◽  
Krista M. Giglio ◽  
David Zamorano-Sánchez ◽  
Jin Hwan Park ◽  
Loni Townsley ◽  
...  
Keyword(s):  
Cell Surface ◽  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Diarrheal Disease ◽  
Cell Attachment ◽  
Surface Display ◽  
Second Messenger ◽  
Bacterial Biofilm ◽  
Content Type ◽  
Regulatory Circuit

ABSTRACT The dinucleotide second messenger c-di-GMP has emerged as a central regulator of reversible cell attachment during bacterial biofilm formation. A prominent cell adhesion mechanism first identified in pseudomonads combines two c-di-GMP-mediated processes: transcription of a large adhesin and its cell surface display via posttranslational proteolytic control. Here, we characterize an orthologous c-di-GMP effector system and show that it is operational in Vibrio cholerae, where it regulates two distinct classes of adhesins. Through structural analyses, we reveal a conserved autoinhibition mechanism of the c-di-GMP receptor that controls adhesin proteolysis and present a structure of a c-di-GMP-bound receptor module. We further establish functionality of the periplasmic protease controlled by the receptor against the two adhesins. Finally, transcription and functional assays identify physiological roles of both c-di-GMP-regulated adhesins in surface attachment and biofilm formation. Together, our studies highlight the conservation of a highly efficient signaling effector circuit for the control of cell surface adhesin expression and its versatility by revealing strain-specific variations. IMPORTANCE Vibrio cholerae, the causative agent of the diarrheal disease cholera, benefits from a sessile biofilm lifestyle that enhances survival outside the host but also contributes to host colonization and infectivity. The bacterial second messenger c-di-GMP has been identified as a central regulator of biofilm formation, including in V. cholerae; however, our understanding of the pathways that contribute to this process is incomplete. Here, we define a conserved signaling system that controls the stability of large adhesion proteins at the cell surface of V. cholerae, which are important for cell attachment and biofilm formation. Insight into the regulatory circuit underlying biofilm formation may inform targeted strategies to interfere with a process that renders this bacterium remarkably adaptable to changing environments.

scholarly journals VpsR Directly Activates Transcription of Multiple Biofilm Genes in Vibrio cholerae

2020 ◽  
Vol 202 (18) ◽  
Author(s):  
Meng-Lun Hsieh ◽  
Christopher M. Waters ◽  
Deborah M. Hinton
Keyword(s):  
Rna Polymerase ◽  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Core Promoter ◽  
Class Ii ◽  
Class I ◽  
Dependent Manner ◽  
Mobility Shift ◽  
Content Type

ABSTRACT Vibrio cholerae biofilm biogenesis, which is important for survival, dissemination, and persistence, requires multiple genes in the Vibrio polysaccharides (vps) operons I and II as well as the cluster of ribomatrix (rbm) genes. Transcriptional control of these genes is a complex process that requires several activators/repressors and the ubiquitous signaling molecule, cyclic di-GMP (c-di-GMP). Previously, we demonstrated that VpsR directly activates RNA polymerase containing σ70 (σ70-RNAP) at the vpsL promoter (PvpsL), which precedes the vps-II operon, in a c-di-GMP-dependent manner by stimulating formation of the transcriptionally active, open complex. Using in vitro transcription, electrophoretic mobility shift assays, and DNase I footprinting, we show here that VpsR also directly activates σ70-RNAP transcription from other promoters within the biofilm formation cluster, including PvpsU, at the beginning of the vps-I operon, PrbmA, at the start of the rbm cluster, and PrbmF, which lies upstream of the divergent rbmF and rbmE genes. In this capacity, we find that VpsR is able to behave both as a class II activator, which functions immediately adjacent/overlapping the core promoter sequence (PvpsL and PvpsU), and as a class I activator, which functions farther upstream (PrbmA and PrbmF). Because these promoters vary in VpsR-DNA binding affinity in the absence and presence of c-di-GMP, we speculate that VpsR’s mechanism of activation is dependent on both the concentration of VpsR and the level of c-di-GMP to increase transcription, resulting in finely tuned regulation. IMPORTANCE Vibrio cholerae, the bacterial pathogen that is responsible for the disease cholera, uses biofilms to aid in survival, dissemination, and persistence. VpsR, which directly senses the second messenger c-di-GMP, is a major regulator of this process. Together with c-di-GMP, VpsR directly activates transcription by RNA polymerase containing σ70 from the vpsL biofilm biogenesis promoter. Using biochemical methods, we demonstrate for the first time that VpsR/c-di-GMP directly activates σ70-RNA polymerase at the first genes of the vps and ribomatrix operons. In this regard, it functions as either a class I or class II activator. Our results broaden the mechanism of c-di-GMP-dependent transcription activation and the specific role of VpsR in biofilm formation.

scholarly journals Cyclic di-GMP Regulates TfoY inVibrio choleraeTo Control Motility by both Transcriptional and Posttranscriptional Mechanisms

2018 ◽  
Vol 200 (7) ◽  
Author(s):  
Benjamin R. Pursley ◽  
Michael M. Maiden ◽  
Meng-Lun Hsieh ◽  
Nicolas L. Fernandez ◽  
Geoffrey B. Severin ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Second Messenger ◽  
Bacterial Motility ◽  
Content Type ◽  
Intracellular Concentrations ◽  
Messenger Molecule

ABSTRACT3′,5′-Cyclic diguanylic acid (c-di-GMP) is a bacterial second messenger molecule that is a key global regulator inVibrio cholerae, but the molecular mechanisms by which this molecule regulates downstream phenotypes have not been fully characterized. One such regulatory factor that may respond to c-di-GMP is the Vc2 c-di-GMP-binding riboswitch that is hypothesized to control the expression of the downstream putative transcription factor TfoY. Although much is known about the physical and structural properties of the Vc2 riboswitch aptamer, the nature of its expression and function inV. choleraehas not been investigated. Here, we show that Vc2 functions as an off switch to inhibit TfoY production at intermediate and high concentrations of c-di-GMP. At low c-di-GMP concentrations, TfoY production is induced to stimulate dispersive motility. We also observed increased transcription oftfoYat high intracellular concentrations of c-di-GMP, but this induction is independent of the Vc2 riboswitch and occurs via transcriptional control of promoters upstream oftfoYby the previously identified c-di-GMP dependent transcription factor VpsR. Our results show that TfoY is induced by c-di-GMP at both low and high intracellular concentrations of c-di-GMP via posttranscriptional and transcriptional mechanisms, respectively. This regulation contributes to the formation of three distinct c-di-GMP signaling states inV. cholerae.IMPORTANCEThe bacterial pathogenVibrio choleraemust transition between life in aquatic environmental reservoirs and life in the gastrointestinal tract. Biofilm formation and bacterial motility, and their control by the second messenger molecule c-di-GMP, play integral roles in this adaptation. Here, we define the third major mechanism by which c-di-GMP controls bacterial motility. This pathway utilizes a noncoding RNA element known as a riboswitch that, when bound to c-di-GMP, inhibits the expression of the transcription factor TfoY. TfoY production switchesV. choleraemotility from a dense to a dispersive state. Our results suggest that the c-di-GMP signaling network ofV. choleraecan exist in at least three distinct states to regulate biofilm formation and motility.

scholarly journals Biofilm Formation by Staphylococcus aureus is Triggered by a Drop in the Levels of the Second Messenger cyclic-di-AMP

2020 ◽  
Author(s):  
Adnan K. Syed ◽  
Christopher R. Vickery ◽  
Taliesin Lenhart ◽  
Eliza Llewellyn ◽  
Suzanne Walker ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Biofilm Formation ◽  
Bacterial Pathogen ◽  
Second Messenger ◽  
Positive Control ◽  
Extracellular Dna ◽  
Dependent Manner ◽  
Accessory Gene ◽  
Accessory Gene Regulator ◽  
The Matrix

AbstractThe bacterial pathogen Staphylococcus aureus forms multicellular communities known as biofilms in which cells are held together by an extracellular matrix. The matrix consists of repurposed cytoplasmic proteins and extracellular DNA. These communities assemble during growth on medium containing glucose, but the intracellular signal for biofilm formation was unknown. Here we present evidence that biofilm formation is triggered by a drop in the levels of the second messenger cyclic-di-AMP. Previous work identified genes needed for the release of extracellular DNA, including genes for the cyclic-di-AMP phosphodiesterase GdpP, the transcriptional regulator XdrA, and the purine salvage enzyme Apt. Using a cyclic-di-AMP riboswitch biosensor and mass spectrometry, we show that the levels of the second messenger drop during biofilm formation in a glucose-dependent manner and that the drop is prevented in mutants of all three genes. Importantly, we also show that expression of the “accessory gene regulator” operon agr is under the positive control of cyclic-di-AMP and that an agr mutation, which is known to promote biofilm formation, bypasses the block in biofilm formation and eDNA release caused by a gdpP mutation. We conclude that the effect of the glucose-dependent drop in c-di-AMP levels is principally mediated by a reduction in agr expression, which in turn promotes biofilm formation.

scholarly journals Response of Vibrio cholerae to Low-Temperature Shifts: CspV Regulation of Type VI Secretion, Biofilm Formation, and Association with Zooplankton

2016 ◽  
Vol 82 (14) ◽  
pp. 4441-4452 ◽  
Author(s):  
Loni Townsley ◽  
Marilou P. Sison Mangus ◽  
Sanjin Mehic ◽  
Fitnat H. Yildiz
Keyword(s):  
Low Temperature ◽  
Vibrio Cholerae ◽  
Causative Agent ◽  
Biofilm Formation ◽  
Cold Shock ◽  
Diarrheal Disease ◽  
Dependent Manner ◽  
Natural Habitats ◽  
Content Type ◽  
Type Vi Secretion

ABSTRACTThe ability to sense and adapt to temperature fluctuation is critical to the aquatic survival, transmission, and infectivity ofVibrio cholerae, the causative agent of the disease cholera. Little information is available on the physiological changes that occur whenV. choleraeexperiences temperature shifts. The genome-wide transcriptional profile ofV. choleraeupon a shift in human body temperature (37°C) to lower temperatures, 15°C and 25°C, which mimic those found in the aquatic environment, was determined. Differentially expressed genes included those involved in the cold shock response, biofilm formation, type VI secretion, and virulence. Analysis of a mutant lacking the cold shock genecspV, which was upregulated >50-fold upon a low-temperature shift, revealed that it regulates genes involved in biofilm formation and type VI secretion. CspV controls biofilm formation through modulation of the second messenger cyclic diguanylate and regulates type VI-mediated interspecies killing in a temperature-dependent manner. Furthermore, a strain lackingcspVhad significant defects for attachment and type VI-mediated killing on the surface of the aquatic crustaceanDaphnia magna. Collectively, these studies reveal thatcspVis a major regulator of the temperature downshift response and plays an important role in controlling cellular processes crucial to the infectious cycle ofV. cholerae.IMPORTANCELittle is known about how human pathogens respond and adapt to ever-changing parameters of natural habitats outside the human host and how environmental adaptation alters dissemination.Vibrio cholerae, the causative agent of the severe diarrheal disease cholera, experiences fluctuations in temperature in its natural aquatic habitats and during the infection process. Furthermore, temperature is a critical environmental signal governing the occurrence ofV. choleraeand cholera outbreaks. In this study, we showed thatV. choleraereprograms its transcriptome in response to fluctuations in temperature, which results in changes to biofilm formation and type VI secretion system activation. These processes in turn impact environmental survival and the virulence potential of this pathogen.

scholarly journals In VitroAnalyses of the Effects of Heparin and Parabens on Candida albicans Biofilms and Planktonic Cells

2011 ◽  
Vol 56 (1) ◽  
pp. 148-153 ◽  
Author(s):  
Marisa H. Miceli ◽  
Stella M. Bernardo ◽  
T. S. Neil Ku ◽  
Carla Walraven ◽  
Samuel A. Lee
Keyword(s):  
Candida Albicans ◽  
Metabolic Activity ◽  
Biofilm Formation ◽  
High Dose ◽  
Dependent Manner ◽  
Planktonic Cells ◽  
Content Type ◽  
Heparin Sodium ◽  
The Individual

ABSTRACTInfections and thromboses are the most common complications associated with central venous catheters. Suggested strategies for prevention and management of these complications include the use of heparin-coated catheters, heparin locks, and antimicrobial lock therapy. However, the effects of heparin onCandida albicansbiofilms and planktonic cells have not been previously studied. Therefore, we sought to determine thein vitroeffect of a heparin sodium preparation (HP) on biofilms and planktonic cells ofC. albicans. Because HP contains two preservatives, methyl paraben (MP) and propyl paraben (PP), these compounds and heparin sodium without preservatives (Pure-H) were also tested individually. The metabolic activity of the mature biofilm after treatment was assessed using XTT [2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide] reduction and microscopy. Pure-H, MP, and PP caused up to 75, 85, and 60% reductions of metabolic activity of the mature preformedC. albicansbiofilms, respectively. Maximal efficacy against the mature biofilm was observed with HP (up to 90%) compared to the individual compounds (P< 0.0001). Pure-H, MP, and PP each inhibitedC. albicansbiofilm formation up to 90%. A complete inhibition of biofilm formation was observed with HP at 5,000 U/ml and higher. When tested against planktonic cells, each compound inhibited growth in a dose-dependent manner. These data indicated that HP, MP, PP, and Pure-H havein vitroantifungal activity againstC. albicansmature biofilms, formation of biofilms, and planktonic cells. Investigation of high-dose heparin-based strategies (e.g., heparin locks) in combination with traditional antifungal agents for the treatment and/or prevention ofC. albicansbiofilms is warranted.

scholarly journals Identification and Characterization of OscR, a Transcriptional Regulator Involved in Osmolarity Adaptation in Vibrio cholerae

2009 ◽  
Vol 191 (13) ◽  
pp. 4082-4096 ◽  
Author(s):  
Nicholas J. Shikuma ◽  
Fitnat H. Yildiz
Keyword(s):  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Transcriptional Regulator ◽  
Dependent Manner ◽  
Genome Wide ◽  
Low Salt ◽  
Adaptation Response ◽  
Matrix Production ◽  
Identification And Characterization

ABSTRACT Vibrio cholerae is a facultative human pathogen. In its aquatic habitat and as it passes through the digestive tract, V. cholerae must cope with fluctuations in salinity. We analyzed the genome-wide transcriptional profile of V. cholerae grown at different NaCl concentrations and determined that the expression of compatible solute biosynthesis and transporter genes, virulence genes, and genes involved in adhesion and biofilm formation is differentially regulated. We determined that salinity modulates biofilm formation, and this response was mediated through the transcriptional regulators VpsR and VpsT. Additionally, a transcriptional regulator controlling an osmolarity adaptation response was identified. This regulator, OscR (osmolarity controlled regulator), was found to modulate the transcription of genes involved in biofilm matrix production and motility in a salinity-dependent manner. oscR mutants were less motile and exhibited enhanced biofilm formation only under low-salt conditions.

Two regulatory factors of Vibrio cholerae activating the mannose-sensitive haemagglutinin pilus expression is important for biofilm formation and colonization in mice

Microbiology ◽  
2021 ◽  
Vol 167 (10) ◽  
Author(s):  
Mengting Shi ◽  
Yue Zheng ◽  
Xianghong Wang ◽  
Zhengjia Wang ◽  
Menghua Yang
Keyword(s):  
Mouse Model ◽  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Type Species ◽  
Wild Type ◽  
Expression Library ◽  
Content Type ◽  
Genomic Expression ◽  
Infant Mouse ◽  
Link Type

Vibrio cholerae the causative agent of cholera, uses a large number of coordinated transcriptional regulatory events to transition from its environmental reservoir to the host intestine, which is its preferred colonization site. Transcription of the mannose-sensitive haemagglutinin pilus (MSHA), which aids the persistence of V. cholerae in aquatic environments, but causes its clearance by host immune defenses, was found to be regulated by a yet unknown mechanism during the infection cycle of V. cholerae . In this study, genomic expression library screening revealed that two regulators, VC1371 and VcRfaH, are able to positively activate the transcription of MSHA operon. VC1371 is localized and active in the cell membrane. Deletion of vc1371 or VcrfaH genes in V. cholerae resulted in less MshA protein production and less efficiency of biofilm formation compared to that in the wild-type strain. An adult mouse model showed that the mutants with vc1371 or VcrfaH deletion colonized less efficiently than the wild-type; the VcrfaH deletion mutant showed less colonization efficiency in the infant mouse model. The findings strongly suggested that the two regulators, namely VC1371 and VcRfaH, which are involved in the regulation of MSHA expression, play an important role in V. cholerae biofilm formation and colonization in mice.

scholarly journals Cyclic Di-GMP Regulates Multiple Cellular Functions in the Symbiotic Alphaproteobacterium Sinorhizobium meliloti

2015 ◽  
Vol 198 (3) ◽  
pp. 521-535 ◽  
Author(s):  
Simon Schäper ◽  
Elizaveta Krol ◽  
Dorota Skotnicka ◽  
Volkhard Kaever ◽  
Rolf Hilker ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Sinorhizobium Meliloti ◽  
Acid Stress ◽  
Second Messenger ◽  
Lifestyle Changes ◽  
Single Domain ◽  
Receptor Protein ◽  
Leguminous Plant ◽  
Content Type

ABSTRACTSinorhizobium melilotiundergoes major lifestyle changes between planktonic states, biofilm formation, and symbiosis with leguminous plant hosts. In many bacteria, the second messenger 3′,5′-cyclic di-GMP (c-di-GMP, or cdG) promotes a sessile lifestyle by regulating a plethora of processes involved in biofilm formation, including motility and biosynthesis of exopolysaccharides (EPS). Here, we systematically investigated the role of cdG inS. melilotiRm2011 encoding 22 proteins putatively associated with cdG synthesis, degradation, or binding. Single mutations in 21 of these genes did not cause evident changes in biofilm formation, motility, or EPS biosynthesis. In contrast, manipulation of cdG levels by overproducing endogenous or heterologous diguanylate cyclases (DGCs) or phosphodiesterases (PDEs) affected these processes and accumulation ofN-Acyl-homoserine lactones in the culture supernatant. Specifically, individual overexpression of theS. melilotigenespleD,SMb20523,SMb20447,SMc01464, andSMc03178encoding putative DGCs and ofSMb21517encoding a single-domain PDE protein had an impact and resulted in increased levels of cdG. Compared to the wild type, anS. melilotistrain that did not produce detectable levels of cdG (cdG0) was more sensitive to acid stress. However, it was symbiotically potent, unaffected in motility, and only slightly reduced in biofilm formation. TheSMc01790-SMc01796locus, homologous to theAgrobacterium tumefaciensuppABCDEFcluster governing biosynthesis of a unipolarly localized polysaccharide, was found to be required for cdG-stimulated biofilm formation, while the single-domain PilZ protein McrA was identified as a cdG receptor protein involved in regulation of motility.IMPORTANCEWe present the first systematic genome-wide investigation of the role of 3′,5′-cyclic di-GMP (c-di-GMP, or cdG) in regulation of motility, biosynthesis of exopolysaccharides, biofilm formation, quorum sensing, and symbiosis in a symbiotic alpha-rhizobial species. Phenotypes of anS. melilotistrain unable to produce cdG (cdG0) demonstrated that this second messenger is not essential for root nodule symbiosis but may contribute to acid tolerance. Our data further suggest that enhanced levels of cdG promote sessility ofS. melilotiand uncovered a single-domain PilZ protein as regulator of motility.

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