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.186.5.1574-1578.2004

Cited by 171 publications

(74 citation statements)

References 28 publications

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“…The main components of V. cholerae biofilms are Vibrio polysaccharide (VPS) and the matrix proteins RbmA, RbmC, and Bap1 (5-9). The transcription of the genes that code for these matrix components and their biosynthetic enzymes is primarily controlled by the transcriptional regulatory proteins VpsR, VpsT, and HapR (10)(11)(12). VpsR and VpsT bind directly to the upstream regulatory regions of the vps-I and vps-II operons and directly activate the expression of vps genes (13).…”

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The LonA Protease Regulates Biofilm Formation, Motility, Virulence, and the Type VI Secretion System in Vibrio cholerae

et al. 2016

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The presence of the Lon protease in all three domains of life hints at its biological importance. The prokaryotic Lon protease is responsible not only for degrading abnormal proteins but also for carrying out the proteolytic regulation of specific protein targets. Posttranslational regulation by Lon is known to affect a variety of physiological traits in many bacteria, including biofilm formation, motility, and virulence. Here, we identify the regulatory roles of LonA in the human pathogen Vibrio cholerae. We determined that the absence of LonA adversely affects biofilm formation, increases swimming motility, and influences intracellular levels of cyclic diguanylate. Whole-genome expression analysis revealed that the message abundance of genes involved in biofilm formation was decreased but that the message abundances of those involved in virulence and the type VI secretion system were increased in a lonA mutant compared to the wild type. We further demonstrated that a lonA mutant displays an increase in type VI secretion system activity and is markedly defective in colonization of the infant mouse. These findings suggest that LonA plays a critical role in the environmental survival and virulence of V. cholerae. IMPORTANCEBacteria utilize intracellular proteases to degrade damaged proteins and adapt to changing environments. The Lon protease has been shown to be important for environmental adaptation and plays a crucial role in regulating the motility, biofilm formation, and virulence of numerous plant and animal pathogens. We find that LonA of the human pathogen V. cholerae is in line with this trend, as the deletion of LonA leads to hypermotility and defects in both biofilm formation and colonization of the infant mouse. In addition, we show that LonA regulates levels of cyclic diguanylate and the type VI secretion system. Our observations add to the known regulatory repertoire of the Lon protease and the current understanding of V. cholerae physiology.

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The LonA Protease Regulates Biofilm Formation, Motility, Virulence, and the Type VI Secretion System in Vibrio cholerae

et al. 2016

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“…Expression of the vps genes encoding the biofilm matrix exopolysaccharide is enhanced at high intracellular c-di-GMP levels due to the induction and increased activity of two c-di-GMP binding regulators, VpsR and VpsT (16,17). VpsR is a homologue of the NtrC subclass of response regulators which binds to the vpsT promoter to activate its transcription (18).…”

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The LuxR-Type Regulator VpsT Negatively Controls the Transcription of rpoS, Encoding the General Stress Response Regulator, in Vibrio cholerae Biofilms

Wang¹,

Ayala²,

Benítez³

et al. 2013

Journal of Bacteriology

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Cholera is a waterborne diarrheal disease caused by Vibrio cholerae strains of serogroups O1 and O139. Expression of the general stress response regulator RpoS and formation of biofilm communities enhance the capacity of V. cholerae to persist in aquatic environments. The transition of V. cholerae between free-swimming (planktonic) and biofilm life-styles is regulated by the second messenger cyclic di-GMP (c-di-GMP). We previously reported that increasing the c-di-GMP pool by overexpression of a diguanylate cyclase diminished RpoS expression. Here we show that c-di-GMP repression of RpoS expression is eliminated by deletion of the genes vpsR and vpsT, encoding positive regulators of biofilm development. To determine the mechanism of this regulation, we constructed a strain expressing a vpsT-FLAG allele from native transcription and translation signals. Increasing the c-di-GMP pool induced vpsT-FLAG expression. The interaction between VpsT-FLAG and the rpoS promoter was demonstrated by chromatin immunoprecipitation. Furthermore, purified VpsT interacted with the rpoS promoter in a c-di-GMP-dependent manner. Primer extension analysis identified two rpoS transcription initiation sites located 43 bp (P1) and 63 bp (P2) upstream of the rpoS start codon. DNase I footprinting showed that the VpsT binding site at the rpoS promoter overlaps the primary P1 transcriptional start site. Deletion of vpsT significantly enhanced rpoS expression in V. cholerae biofilms that do not make HapR. This result suggests that VpsT and c-di-GMP contribute to the transcriptional silencing of rpoS in biofilms prior to cells entering the quorum-sensing mode.

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“…VpsR is required for biofilm formation, as disruption of vpsR abolishes biofilm formation (25). The second positive regulator of biofilm formation is VpsT; its disruption reduces the biofilm-forming capacity of V. cholerae (26). CarR negatively regulates expression of vpsR and vpsT (18).…”

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Polymyxin B Resistance and Biofilm Formation in Vibrio cholerae Are Controlled by the Response Regulator CarR

et al. 2015

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Two-component systems play important roles in the physiology of many bacterial pathogens. Vibrio cholerae's CarRS two-component regulatory system negatively regulates expression of vps (Vibrio polysaccharide) genes and biofilm formation. In this study, we report that CarR confers polymyxin B resistance by positively regulating expression of the almEFG genes, whose products are required for glycine and diglycine modification of lipid A. We determined that CarR directly binds to the regulatory region of the almEFG operon. Similarly to a carR mutant, strains lacking almE, almF, and almG exhibited enhanced polymyxin B sensitivity. We also observed that strains lacking almE or the almEFG operon have enhanced biofilm formation. Our results reveal that CarR regulates biofilm formation and antimicrobial peptide resistance in V. cholerae.

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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 171 publications

References 28 publications

The LonA Protease Regulates Biofilm Formation, Motility, Virulence, and the Type VI Secretion System in Vibrio cholerae

The LonA Protease Regulates Biofilm Formation, Motility, Virulence, and the Type VI Secretion System in Vibrio cholerae

The LuxR-Type Regulator VpsT Negatively Controls the Transcription of rpoS, Encoding the General Stress Response Regulator, in Vibrio cholerae Biofilms

Polymyxin B Resistance and Biofilm Formation in Vibrio cholerae Are Controlled by the Response Regulator CarR

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