VpsT Is a Transcriptional Regulator Required for Expression of
            <i>vps</i>
            Biosynthesis Genes and the Development of Rugose Colonial Morphology in
            <i>Vibrio cholerae</i>
            O1 El Tor

Casper-Lindley, Catharina; Yildiz, Fitnat H.

doi:10.1128/jb.00835-06

Cited by 68 publications

(111 citation statements)

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“…We were intrigued by our identification of vpsT as a VqmR target because vpsT encodes a major transcriptional regulator of biofilm formation. At low cell density, VpsT activates the expression of genes required for production of vibrio polysaccharide (vps), and, thus, mutation of vpsT strongly inhibits biofilm formation (36). Transcription of vpsT is itself activated by another biofilm regulator, VpsR (37).…”

Section: C H O Le R a E V H A R V E Y I V A N G U Il La R U Mmentioning

confidence: 99%

Differential RNA-seq of Vibrio cholerae identifies the VqmR small RNA as a regulator of biofilm formation

Papenfort¹,

Förstner

Cong³

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

196

265

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Quorum sensing (QS) is a process of cell-to-cell communication that enables bacteria to transition between individual and collective lifestyles. QS controls virulence and biofilm formation in Vibrio cholerae, the causative agent of cholera disease. Differential RNA sequencing (RNA-seq) of wild-type V. cholerae and a locked low-cell-density QS-mutant strain identified 7,240 transcriptional start sites with ∼47% initiated in the antisense direction. A total of 107 of the transcripts do not appear to encode proteins, suggesting they specify regulatory RNAs. We focused on one such transcript that we name VqmR. vqmR is located upstream of the vqmA gene encoding a DNA-binding transcription factor. Mutagenesis and microarray analyses demonstrate that VqmA activates vqmR transcription, that vqmR encodes a regulatory RNA, and VqmR directly controls at least eight mRNA targets including the rtx (repeats in toxin) toxin genes and the vpsT transcriptional regulator of biofilm production. We show that VqmR inhibits biofilm formation through repression of vpsT. Together, these data provide to our knowledege the first global annotation of the transcriptional start sites in V. cholerae and highlight the importance of posttranscriptional regulation for collective behaviors in this human pathogen.Q uorum sensing (QS) is a process of bacterial cell-to-cell communication that relies on the production, release, accumulation, and population-wide detection of extracellular signal molecules called autoinducers. Processes controlled by QS are unproductive when undertaken by an individual bacterium but become effective when performed in unison by the group. In the major human pathogen, Vibrio cholerae, QS orchestrates processes including biofilm formation and virulence factor production (1). In the V. cholerae QS circuit, at low cell density (LCD), LuxO∼P activates transcription of genes encoding four small regulatory RNAs (sRNAs), Qrr1-4, which promote translation of the low cell density master QS regulator, AphA, and repress translation of HapR, the high cell density (HCD) master QS regulator (2, 3). AphA directs the gene expression program for V. cholerae cells to act as individuals. At high cell density, in the presence of autoinducers, LuxO is dephosphorylated and inactivated (4). The Qrr sRNAs are not transcribed, AphA is not produced, and by contrast, the hapR mRNA is translated into HapR protein. HapR controls the gene expression program underpinning collective behaviors (5, 6). Thus, the absence or presence of the Qrr sRNAs directs whether or not V. cholerae engages in QS. The Qrr sRNAs belong to the family of Hfq-binding sRNAs that regulate gene expression through base pairing with target mRNAs (7).An explosion in the discovery of noncoding transcripts, including sRNAs, has occurred due to recently developed transcriptomic technologies such as high-throughput sequencing of cDNAs, e.g., RNA sequencing (RNA-seq). (8). Major advantages of RNA-seq over conventional methods include high sensitivity for low abundance transcripts, ind...

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Section: C H O Le R a E V H A R V E Y I V A N G U Il La R U Mmentioning

confidence: 99%

Differential RNA-seq of Vibrio cholerae identifies the VqmR small RNA as a regulator of biofilm formation

Papenfort¹,

Förstner

Cong³

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

196

265

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“…In V. cholerae, the two central regulators of vps (vibrio poly- (47,356). However, under flowthrough conditions, which reduce cell density effects such as accumulation of autoinducers, a vpsT mutant is able to form a well-developed biofilm, suggesting that vpsT regulation of biofilm formation is more sensitive to cell density effects (25).…”

mentioning

confidence: 99%

“…Furthermore, the quorum-sensing regulator HapR was shown to directly bind to the vpsT but not the vpsR promoter, suggesting that quorum sensing reduces vpsT gene transcription at least partially as a result of direct repression by HapR (343). VpsT and VpsR positively regulate their own expression as well as that of each other (25,47). Various expression profiling studies have shown that increased c-di-GMP levels, overexpression of DGCs, and deletion of PDEAs increase vpsT gene transcription, suggesting that vpsT, either indirectly or directly, is a downstream target of c-di-GMP signaling pathways (25,26,47,164,202,357).…”

mentioning

confidence: 99%

Signals, Regulatory Networks, and Materials That Build and Break Bacterial Biofilms

Karatan

Watnick

2009

Microbiol Mol Biol Rev

846

690

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SUMMARY Biofilms are communities of microorganisms that live attached to surfaces. Biofilm formation has received much attention in the last decade, as it has become clear that virtually all types of bacteria can form biofilms and that this may be the preferred mode of bacterial existence in nature. Our current understanding of biofilm formation is based on numerous studies of myriad bacterial species. Here, we review a portion of this large body of work including the environmental signals and signaling pathways that regulate biofilm formation, the components of the biofilm matrix, and the mechanisms and regulation of biofilm dispersal.

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“…It is thought that the adeptness of Vibrio cells at changing back and forth from either phenotypic variant would favor the variant derivative that is more fit for survival under the prevailing environment conditions, such as those encountered in a human host or on an environmental surface. Regulation of rugosity seems to be multifactorial and highly complex (5,17,26,36,37). Although there are some similarities, great differences are observed among organisms capable of expressing rugosity (3,36,37).…”

Section: Discussionmentioning

confidence: 99%

Rugosity in Grimontia hollisae

Curtis

Kothary

Blodgett

et al. 2007

Appl Environ Microbiol

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Grimontia hollisae, formerly Vibrio hollisae, produces both smooth and rugose colonial variants. The rugose colony phenotype is characterized by wrinkled colonies producing copious amounts of exopolysaccharide. Cells from a rugose colony grown at 30°C form rugose colonies, while the same cells grown at 37°C form smooth colonies, which are characterized by a nonwrinkled, uncrannied appearance. Stress response studies revealed that after exposure to bleach for 30 min, rugose survivors outnumbered smooth survivors.

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VpsT Is a Transcriptional Regulator Required for Expression of vps Biosynthesis Genes and the Development of Rugose Colonial Morphology in Vibrio cholerae O1 El Tor

Cited by 68 publications

References 0 publications

Differential RNA-seq of Vibrio cholerae identifies the VqmR small RNA as a regulator of biofilm formation

Differential RNA-seq of Vibrio cholerae identifies the VqmR small RNA as a regulator of biofilm formation

Signals, Regulatory Networks, and Materials That Build and Break Bacterial Biofilms

Rugosity in Grimontia hollisae

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