Publication:
Moonlighting bacteriophage proteins derepress staphylococcal pathogenicity islands

dc.contributor.authorTormo Más, María Ángeles
dc.contributor.authorMir, Ignacio
dc.contributor.authorShrestha, Archana
dc.contributor.authorTallent, Sandra M.
dc.contributor.authorCampoy Sánchez, Susana
dc.contributor.authorLasa Uzcudun, Íñigo
dc.contributor.authorBarbé, Jordi
dc.contributor.authorNovick, Richard P.
dc.contributor.authorChristie, Gail E.
dc.contributor.authorPenadés, José R.
dc.contributor.departmentIdAB. Instituto de Agrobiotecnología / Agrobioteknologiako Institutuaes_ES
dc.date.accessioned2019-04-03T07:22:26Z
dc.date.available2019-04-03T07:22:26Z
dc.date.issued2010
dc.description.abstractStaphylococcal 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.en
dc.description.sponsorshipThis 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.en
dc.format.extent10 p.
dc.format.mimetypeapplication/pdfen
dc.identifier.doi10.1038/nature09065
dc.identifier.issn1476-4687 (Electronic)
dc.identifier.urihttps://academica-e.unavarra.es/handle/2454/32799
dc.language.isoengen
dc.publisherNature Researchen
dc.relation.ispartofNature, volume 465, pages 779–782 (10 June 2010)en
dc.relation.publisherversionhttps://doi.org/10.1038/nature09065
dc.rights©2010 Macmillan Publishers Limited. All rights reserved.en
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.subjectStaphylococcal pathogenicity islandsen
dc.titleMoonlighting bacteriophage proteins derepress staphylococcal pathogenicity islandsen
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/acceptedVersionen
dc.type.versionVersión aceptada / Onetsi den bertsioaes
dspace.entity.typePublication
relation.isAuthorOfPublicationc654d104-1ae2-41cf-9215-4b4bed3e5ea6
relation.isAuthorOfPublication.latestForDiscoveryc654d104-1ae2-41cf-9215-4b4bed3e5ea6

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