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    Moonlighting bacteriophage proteins derepress staphylococcal pathogenicity islands

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    Date
    2010
    Author
    Tormo Más, María Ángeles 
    Mir, Ignacio 
    Shrestha, Archana 
    Tallent, Sandra M. 
    Campoy Sánchez, Susana 
    Lasa Uzcudun, Íñigo Upna Orcid
    Barbé, Jordi 
    Novick, Richard P. 
    Christie, Gail E. 
    Penadés, José R. 
    Version
    Acceso abierto / Sarbide irekia
    Type
    Artículo / Artikulua
    Version
    Versión aceptada / Onetsi den bertsioa
    Impact
     
     
     
    10.1038/nature09065
     
     
     
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    Abstract
    Staphylococcal superantigen-carrying pathogenicity islands (SaPIs) are discrete, chromosomally integrated units of ∼15 kilobases that are induced by helper phages to excise and replicate. SaPI DNA is then efficiently encapsidated in phage-like infectious particles, leading to extremely high frequencies of intra- as well as intergeneric transfer1,2,3. In the absence of helper phage lytic growth, t ... [++]
    Staphylococcal superantigen-carrying pathogenicity islands (SaPIs) are discrete, chromosomally integrated units of ∼15 kilobases that are induced by helper phages to excise and replicate. SaPI DNA is then efficiently encapsidated in phage-like infectious particles, leading to extremely high frequencies of intra- as well as intergeneric transfer1,2,3. In the absence of helper phage lytic growth, the island is maintained in a quiescent prophage-like state by a global repressor, Stl, which controls expression of most of the SaPI genes4. Here we show that SaPI derepression is effected by a specific, non-essential phage protein that binds to Stl, disrupting the Stl–DNA complex and thereby initiating the excision-replication-packaging cycle of the island. Because SaPIs require phage proteins to be packaged5,6, this strategy assures that SaPIs will be transferred once induced. Several different SaPIs are induced by helper phage 80α and, in each case, the SaPI commandeers a different non-essential phage protein for its derepression. The highly specific interactions between different SaPI repressors and helper-phage-encoded antirepressors represent a remarkable evolutionary adaptation involved in pathogenicity island mobilization. [--]
    Subject
    Staphylococcal pathogenicity islands
    Publisher
    Nature Research
    Published in
    Nature, volume 465, pages 779–782 (10 June 2010)
    Departament
    IdAB – Instituto de Agrobiotecnología / Agrobioteknologiako Institutua
    Publisher version
    https://doi.org/10.1038/nature09065
    URI
    https://hdl.handle.net/2454/32799
    Sponsorship
    This work was supported by grants Consolider-Ingenio CSD2009-00006, BIO2005-08399-C02-02, BIO2008-05284-C02-02 and BIO2008-00642-E/C from the Ministerio de Ciencia e Innovación (MICINN), grants from the Cardenal Herrera-CEU University (PRCEU-UCH25/08 and Copernicus program), from the Conselleria de Agricultura, Pesca i Alimentació (CAPiA) and from the Generalitat Valenciana (ACOMP07/258) to J.R.P.; grants BFU2008-01078 from the MICINN and 2009SGR1106 from the Generalitat de Catalunya to J.B.; NIH grant R21AI067654 and a grant-in-aid from the A. D. Williams Trust and the Baruch Foundation Trust to G.E.C.; and NIH grant R01AI022159-23A2 to R.P.N. Fellowship support for M.A.T.-M. from the Generalitat Valenciana is gratefully acknowledged.
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