Staying Alive:
            <i>Vibrio cholerae</i>
            ’s Cycle of Environmental Survival, Transmission, and Dissemination

Conner, Jenna G.; Teschler, Jennifer K.; Jones, Christopher J.; Yildiz, Fitnat H.

doi:10.1128/microbiolspec.vmbf-0015-2015

Cited by 114 publications

(72 citation statements)

References 240 publications

(348 reference statements)

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“…Biofilm matrix production is regulated by c-di-GMP at the transcriptional level by two key transcriptional activators, VpsR (VC0665) and VpsT (VCA0952) [30] (Fig 3C). VpsR directly activates the expression of VPS biosynthesis genes and genes encoding matrix proteins [31].…”

Section: Introductionmentioning

confidence: 99%

The ins and outs of cyclic di-GMP signaling in Vibrio cholerae

Conner

Zamorano‐Sánchez

Park

et al. 2017

Current Opinion in Microbiology

129

124

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The second messenger nucleotide cyclic dimeric guanosine monophosphate (c-di-GMP) governs many cellular processes in the facultative human pathogen Vibrio cholerae. This organism copes with changing environmental conditions in aquatic environments and during transitions to and from human hosts. Modulation of c-di-GMP allows V. cholerae to shift between motile and sessile stages of life, thus allowing adaptation to stressors and environmental conditions during its transmission cycle. The V. cholerae genome encodes a large set of proteins predicted to degrade and produce c-di-GMP. A subset of these enzymes has been demonstrated to control cellular processes – particularly motility, biofilm formation, and virulence – through transcriptional, post-transcriptional, and translational mechanisms. Recent studies have identified and characterized enzymes that modulate or sense c-di-GMP levels and have lead towards mechanistic understanding of c-di-GMP regulatory circuits in V. cholerae.

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Section: Introductionmentioning

confidence: 99%

The ins and outs of cyclic di-GMP signaling in Vibrio cholerae

Conner

Zamorano‐Sánchez

Park

et al. 2017

Current Opinion in Microbiology

129

124

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“…Vibrio cholerae of serogroup O1 and O139, the causative agent of the diarrheal disease cholera, expresses multiple pili, which mediate its adherence to different substrata in the aquatic environment and the human small intestine (1). For instance, the mannose-sensitive hemagglutinin (MSHA) participates in V. cholerae attachment to borosilicate (2, 3) and to the exoskeleton of planktonic crustacean (4); the N-acetylglucosamine binding protein GbpA mediates attachment of vibrios to chitin and intestinal mucin (5, 6); the chitin-regulated pilus ChiRP promotes attachment to chitinous surfaces (7) and the toxin-coregulated pilus (TCP) mediates attachment to cultured intestinal cells, the intestinal microvilli and microcolony formation (8–10).…”

Section: Introductionmentioning

confidence: 99%

“…V. cholerae attachment to chitinous surfaces in aquatic ecosystems can progress to the formation of biofilm communities that can persist for longer periods in the environment (1). In the small intestine, initial attachment of vibrios to the protective mucus layer can be followed by multiple cycles of mucus gel penetration, adherence to the microvilli, microcolony formation and detachment [reviewed in (14, 15)].…”

Section: Introductionmentioning

confidence: 99%

Flagellar motility, extracellular proteases and Vibrio cholerae detachment from abiotic and biotic surfaces

Mewborn

Benítez

Silva

2017

Microbial Pathogenesis

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Vibrio cholerae of serogroups O1 and O139, the causative agent of Asiatic cholera, continues to be a major global health threat. This pathogen utilizes substratum-specific pili to attach to distinct surfaces in the aquatic environment and the human small intestine and detaches when conditions become unfavorable. Both attachment and detachment are critical to bacterial environmental survival, pathogenesis and disease transmission. However, the factors that promote detachment are less understood. In this study, we examine the role of flagellar motility and hemagglutinin/protease (HapA) in vibrio detachment from a non-degradable abiotic surface and from the suckling mouse intestine. Flagellar motility facilitated V. cholerae detachment from abiotic surfaces. HapA had no effect on the stability of biofilms formed on abiotic surfaces despite representing > 50 % of the proteolytic activity present in the extracellular matrix. We developed a balanced lethal plasmid system to increase the bacterial cyclic diguanylate (c-di-GMP) pool late in infection, a condition that represses motility and HapA expression. Increasing the c-di-GMP pool enhanced V. cholerae colonization of the suckling mouse intestine. The c-di-GMP effect was fully abolished in hapA isogenic mutants. These results suggest that motility facilitates detachment in a substratum-independent manner. Instead, HapA appears to function as a substratum-specific detachment factor.

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“…Biofilm formation in Vibrio cholerae is a highly regulated process, controlled by the transcriptional activators VpsR, VpsT and AphA, the transcriptional repressors HapR and H-NS, small regulatory RNAs, alternative sigma factors (RpoS, RpoN and RpoE), and small nucleotide signalling (c-di-GMP, cAMP, ppGpp). Specific environmental signals such as changes in salinity, osmolarity, nutrient availability, phosphate limitation, Ca2+ levels, iron availability, and presence of polyamines (spermidine and norspermidine), indole or bile 14,15 can also affect biofilm formation. Within this complex regulatory network, VpsR and VpsT, whose regulons extensively overlap 16 , are the main transcriptional activators of the vpsI and vpsII clusters and the rbmA, rbmC and bap1 genes encoding the matrix proteins 17 .…”

Section: Introductionmentioning

confidence: 99%

A temperature-dependent translational switch controls biofilm development inVibrio cholerae

Santos

Blake

Sit

et al. 2020

Preprint

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16The gastrointestinal pathogen Vibrio cholerae frequently forms biofilms during its life 17 cycle. Biofilm formation is vital for protection against environmental stresses and is 18 thought to facilitate intestinal colonization. Adaptation to temperature is crucial for V. 19 cholerae survival, as the pathogen is exposed to seasonal temperature variations in 20 the aquatic environment, and temperature fluctuations during host-environment 21 transitions. Here, we show that V. cholerae strains naturally lacking the master biofilm 22 transcriptional regulator HapR are unable to develop colony rugosity at low 23 temperatures. We find that BipA, a ribosome-associated GTPase, accounts for this 24 temperature-dependent control of biofilm formation by repressing translation of the 25 primary biofilm transcriptional activators VpsR and VpsT at low temperatures. In vitro 26 studies demonstrate that low temperatures influence BipA structural conformation and 27 decrease its sensitivity to proteolysis. Proteomic analyses reveal that BipA exerts 28 temperature-dependent control over >200 proteins in V. cholerae involved in a 29 multitude of cell processes, including biofilm assembly. Our study reveals a 30 remarkable new facet of the complex V. cholerae biofilm regulatory cascade and 31suggests that combined transcriptional-translational control could be a common 32 mechanism by which bacteria adapt to environmental flux.A common strategy of bacteria for adaptation and survival to changing environmental 35 conditions is the formation of biofilms: bacterial communities enclosed in an 36 extracellular matrix. Vibrio cholerae, the causative agent of the severe diarrhoeal 37 disease cholera, forms biofilms both in biotic and abiotic surfaces in the aquatic 38 environment that inhabits 1-3 and also in the intestine of the human host 4,5 . The 39 formation of biofilms enhances persistence of V. cholerae, since it provides protection 40 against environmental insults, predators and stress conditions and allows a better 41 access to nutrients 3 . There is some evidence indicating that biofilm-formation capacity 42 is critical for intestinal colonization 5 and biofilms have also been linked to a 43 hyperinfectious phenotype 6 . 44V. cholerae's biofilm is primarily composed of VPS (Vibrio polysaccharide), matrix 45 proteins (RbmA, RbmC and Bap1) and extracellular DNA 7-13 . The genes encoding the 46 activities for the production of VPS, grouped in the vpsI and vpsII clusters, and the 47 genes encoding the RbmA and RbmC matrix proteins, located in the rbm cluster 48 between vpsI and vpsII clusters, form the so-called V. cholerae biofilm-matrix cluster 49 (VcBMC) 7-10 . 50 Biofilm formation inVibrio cholerae is a highly regulated process, controlled by the 51 transcriptional activators VpsR, VpsT and AphA, the transcriptional repressors HapR 52 and H-NS, small regulatory RNAs, alternative sigma factors (RpoS, RpoN and RpoE), 53 and small nucleotide signalling (c-di-GMP, cAMP, ppGpp). Specific environmental 54 signals such as changes...

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Staying Alive: Vibrio cholerae ’s Cycle of Environmental Survival, Transmission, and Dissemination

Cited by 114 publications

References 240 publications

The ins and outs of cyclic di-GMP signaling in Vibrio cholerae

The ins and outs of cyclic di-GMP signaling in Vibrio cholerae

Flagellar motility, extracellular proteases and Vibrio cholerae detachment from abiotic and biotic surfaces

A temperature-dependent translational switch controls biofilm development inVibrio cholerae

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