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    A new regulator of pathogenicity (bvlR) is required for full virulence and tight microcolony formation in Pseudomonas aeruginosa

    Access Status
    Open access via publisher
    Authors
    McCarthy, R.
    Mooij, M.
    Reen, F.
    Lesouhaitier, O.
    O'Gara, Fergal
    Date
    2014
    Type
    Journal Article
    
    Metadata
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    Citation
    McCarthy, R. and Mooij, M. and Reen, F. and Lesouhaitier, O. and O'Gara, F. 2014. A new regulator of pathogenicity (bvlR) is required for full virulence and tight microcolony formation in Pseudomonas aeruginosa. Microbiology. 160 Pt. 7: pp. 1488-1500.
    Source Title
    Microbiology
    DOI
    10.1099/mic.0.075291-0
    ISSN
    1350-0872
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/33935
    Collection
    • Curtin Research Publications
    Abstract

    LysR-type transcriptional regulators (LTTRs) are the most common family of transcriptional regulators found in the opportunistic pathogen Pseudomonas aeruginosa. They are known to regulate a wide variety of virulence determinants and have emerged recently as positive global regulators of pathogenicity in a broad spectrum of important bacterial pathogens. However, in spite of their key role in modulating expression of key virulence determinants underpinning pathogenic traits associated with the process of infection, surprisingly few are found to be transcriptionally altered by contact with host cells. BvlR (PA14_26880) an LTTR of previously unknown function, has been shown to be induced in response to host cell contact, and was therefore investigated for its potential role in virulence. BvlR expression was found to play a pivotal role in the regulation of acute virulence determinants such as type III secretion system and exotoxin A production. BvlR also played a key role in P. aeruginosa pathogenicity within the Caenorhabditis elegans acute model of infection. Loss of BvlR led to an inability to form tight microcolonies, a key step in biofilm formation in the cystic fibrosis lung, although surface attachment was increased. Unusually for LTTRs, BvlR was shown to exert its influence through the transcriptional repression of many genes, including the virulence-associated cupA and alg genes. This highlights the importance of BvlR as a new virulence regulator in P. aeruginosa with a central role in modulating key events in the pathogen–host interactome.

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