Erratum for Beck et al., “Cra and cAMP Receptor Protein Have Opposing Roles in the Regulation of
            fruB
            in Vibrio cholerae”

ABSTRACT Vibrio cholerae is a facultative human pathogen. The ability of V. cholerae to form biofilms is crucial for its survival in aquatic habitats between epidemics and is advantageous for host-to-host transmission during epidemics. Formation of mature biofilms requires the production of extracellular matrix components, including Vibrio polysaccharide (VPS) and matrix proteins. Biofilm formation is positively controlled by the transcriptional regulators VpsR and VpsT and is negatively regulated by the quorum-sensing transcriptional regulator HapR, as well as the cyclic AMP (cAMP)-cAMP receptor protein (CRP) regulatory complex. Transcriptome analysis of cyaA (encoding adenylate cyclase) and crp (encoding cAMP receptor protein) deletion mutants revealed that cAMP-CRP negatively regulates transcription of both VPS biosynthesis genes and genes encoding biofilm matrix proteins. Further mutational and expression analysis revealed that cAMP-CRP negatively regulates transcription of vps genes indirectly through its action on vpsR transcription. However, negative regulation of the genes encoding biofilm matrix proteins by cAMP-CRP can also occur independent of VpsR. Transcriptome analysis also revealed that cAMP-CRP regulates the expression of a set of genes encoding diguanylate cyclases (DGCs) and phosphodiesterases. Mutational and phenotypic analysis of the differentially regulated DGCs revealed that a DGC, CdgA, is responsible for the increase in biofilm formation in the Δcrp mutant, showing the connection between of cyclic di-GMP and cAMP signaling in V. cholerae.

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Sequence and functional analysis of the gene encoding Vibrio cholerae cAMP receptor protein

Gene ◽

10.1016/s0378-1119(97)00331-4 ◽

1997 ◽

Vol 198 (1-2) ◽

pp. 297-303 ◽

Cited By ~ 11

Author(s):

Karen Skorupski ◽

Ronald K Taylor

Keyword(s):

Functional Analysis ◽

Vibrio Cholerae ◽

Receptor Protein ◽

Camp Receptor Protein ◽

Gene Encoding ◽

Camp Receptor

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cAMP Receptor Protein ControlsVibrio choleraeGene Expression in Response to Host Colonization

mBio ◽

10.1128/mbio.00966-18 ◽

2018 ◽

Vol 9 (4) ◽

Cited By ~ 15

Author(s):

Jainaba Manneh-Roussel ◽

James R. J. Haycocks ◽

Andrés Magán ◽

Nicolas Perez-Soto ◽

Kerstin Voelz ◽

...

Keyword(s):

Gene Expression ◽

Transcription Factors ◽

Vibrio Cholerae ◽

Expression Patterns ◽

Lifestyle Changes ◽

Receptor Protein ◽

Camp Receptor Protein ◽

Host Colonization ◽

Content Type ◽

Camp Receptor

ABSTRACTThe bacteriumVibrio choleraeis native to aquatic environments and can switch lifestyles to cause disease in humans. Lifestyle switching requires modulation of genetic systems for quorum sensing, intestinal colonization, and toxin production. Much of this regulation occurs at the level of gene expression and is controlled by transcription factors. In this work, we have mapped the binding of cAMP receptor protein (CRP) and RNA polymerase across theV. choleraegenome. We show that CRP is an integral component of the regulatory network that controls lifestyle switching. Focusing on a locus necessary for toxin transport, we demonstrate CRP-dependent regulation of gene expression in response to host colonization. Examination of further CRP-targeted genes reveals that this behavior is commonplace. Hence, CRP is a key regulator of manyV. choleraegenes in response to lifestyle changes.IMPORTANCECholera is an infectious disease that is caused by the bacteriumVibrio cholerae. Best known for causing disease in humans, the bacterium is most commonly found in aquatic ecosystems. Hence, humans acquire cholera following ingestion of food or water contaminated withV. cholerae. Transition between an aquatic environment and a human host triggers a lifestyle switch that involves reprogramming ofV. choleraegene expression patterns. This process is controlled by a network of transcription factors. In this paper, we show that the cAMP receptor protein (CRP) is a key regulator ofV. choleraegene expression in response to lifestyle changes.

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Cra and cAMP Receptor Protein Have Opposing Roles in the Regulation of fruB in Vibrio cholerae

Journal of Bacteriology ◽

10.1128/jb.00044-21 ◽

2021 ◽

Vol 203 (10) ◽

Author(s):

Christina Beck ◽

Sayde Perry ◽

Daniel M. Stoebel ◽

Jane M. Liu

Keyword(s):

Vibrio Cholerae ◽

Molecular Mechanisms ◽

Carbon Sources ◽

Receptor Protein ◽

Camp Receptor Protein ◽

Phosphotransferase System ◽

Content Type ◽

Catabolite Repressor ◽

Available Carbon ◽

Camp Receptor

ABSTRACT The Gram-negative bacterium Vibrio cholerae adapts to changes in the environment by selectively producing the necessary machinery to take up and metabolize available carbohydrates. The import of fructose by the fructose-specific phosphoenolpyruvate (PEP) phosphotransferase system (PTS) is of particular interest because of its putative connection to cholera pathogenesis and persistence. Here, we describe the expression and regulation of fruB, which encodes an EIIA-FPr fusion protein as part of the fructose-specific PTS in V. cholerae. Using a series of transcriptional reporter fusions and additional biochemical and genetic assays, we identified Cra (catabolite repressor/activator) and cAMP receptor protein (CRP) as regulators of fruB expression and determined that this regulation is dependent upon the presence or absence of PTS sugars. Cra functions as a repressor, downregulating fruB expression in the absence of fructose when components of PTSFru are not needed. CRP functions as an activator of fruB expression. We also report that Cra and CRP can affect fruB expression independently; however, CRP can modulate cra expression in the presence of fructose and glucose. Evidence from this work provides the foundation for continued investigations into PTSFru and its relationship to the V. cholerae life cycle. IMPORTANCE Vibrio cholerae is the causative agent of cholera disease. While current treatments of care are accessible, we still lack an understanding of the molecular mechanisms that allow V. cholerae to survive in both aquatic reservoirs and the human small intestine, where pathogenesis occurs. Central to V. cholerae’s survival is its ability to use available carbon sources. Here, we investigate the regulation of fruB, which encodes a protein central to the import and metabolism of fructose. We show that fruB expression is controlled by the transcriptional regulators Cra and CRP. This work contributes toward a clearer understanding of how carbon source availability impacts the physiology and, potentially, the persistence of the pathogen.

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The Cyclic AMP (cAMP)-cAMP Receptor Protein Signaling System Mediates Resistance of Vibrio cholerae O1 Strains to Multiple Environmental Bacteriophages

Applied and Environmental Microbiology ◽

10.1128/aem.00008-10 ◽

2010 ◽

Vol 76 (13) ◽

pp. 4233-4240 ◽

Cited By ~ 11

Author(s):

M. Shamim Hasan Zahid ◽

T. M. Zaved Waise ◽

M. Kamruzzaman ◽

Amar N. Ghosh ◽

G. Balakrish Nair ◽

...

Keyword(s):

Cyclic Amp ◽

Vibrio Cholerae ◽

Parent Strain ◽

Diarrheal Disease ◽

Indicator Strain ◽

Receptor Protein ◽

Camp Receptor Protein ◽

Selective Enrichment ◽

Camp Receptor ◽

Bacterial Genes

ABSTRACT Toxigenic Vibrio cholerae, the causative agent of the epidemic diarrheal disease cholera, interacts with diverse environmental bacteriophages. These interactions promote genetic diversity or cause selective enrichment of phage-resistant bacterial clones. To identify bacterial genes involved in mediating the phage-resistant phenotype, we screened a transposon insertion library of V. cholerae O1 El Tor biotype strain C6706 to identify mutants showing altered susceptibility to a panel of phages isolated from surface waters in Bangladesh. Mutants with insertion in cyaA or crp genes encoding adenylate cyclase or cyclic AMP (cAMP) receptor protein (CRP), respectively, were susceptible to a phage designated JSF9 to which the parent strain was completely resistant. Application of the cyaA mutant as an indicator strain in environmental phage monitoring enhanced phage detection, and we identified 3 additional phages to which the parent strain was resistant. Incorporation of the cyaA or crp mutations into other V. cholerae O1 strains caused similar alterations in their phage susceptibility patterns, and the susceptibility correlated with the ability of the bacteria to adsorb these phages. Our results suggest that cAMP-CRP-mediated downregulation of phage adsorption may contribute to a mechanism for the V. cholerae O1 strains to survive predation by multiple environmental phages. Furthermore, the cyaA or crp mutant strains may be used as suitable indicators in monitoring cholera phages in the water.

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Environmental Signals Controlling Production of Hemagglutinin/Protease in Vibrio cholerae

Infection and Immunity ◽

10.1128/iai.69.10.6549-6553.2001 ◽

2001 ◽

Vol 69 (10) ◽

pp. 6549-6553 ◽

Cited By ~ 70

Author(s):

Jorge A. Benitez ◽

Anisia J. Silva ◽

Richard A. Finkelstein

Keyword(s):

Vibrio Cholerae ◽

Deletion Mutant ◽

Receptor Protein ◽

Intracellular Camp ◽

Wild Type ◽

Camp Receptor Protein ◽

Environmental Signals ◽

Camp Receptor ◽

Camp Levels

ABSTRACT Vibrio cholerae hemagglutinin/protease (Hap) was induced upon nutrient limitation and strongly repressed by glucose. Hap was not produced in a mutant defective in the cyclic AMP (cAMP) receptor protein, suggesting that intracellular cAMP levels mediate Hap expression. No difference was found in Hap production between anrpoS deletion mutant and its isogenic wild-type precursor, indicating that the alternate ςs factor is not essential for Hap expression. Based on these and previous results, we discuss the role of Hap in the pathogenesis of cholera.

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