SaPI operon I is required for SaPI packaging and is controlled by LexA

Authors

  • Carles Úbeda,

    1. Centro de Investigación y Tecnología Animal, Instituto Valenciano de Investigaciones Agrarias (CITA-IVIA), Apdo. 187, 12.400 Segorbe, Castellón, Spain.
    2. Departamento de Química, Bioquímica y Biología Molecular, Universidad Cardenal Herrera-CEU, 46113 Moncada, Valencia, Spain.
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    • Carles Úbeda and Elisa Maiques contributed equally to this work.

  • Elisa Maiques,

    1. Centro de Investigación y Tecnología Animal, Instituto Valenciano de Investigaciones Agrarias (CITA-IVIA), Apdo. 187, 12.400 Segorbe, Castellón, Spain.
    2. Departamento de Química, Bioquímica y Biología Molecular, Universidad Cardenal Herrera-CEU, 46113 Moncada, Valencia, Spain.
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    • Carles Úbeda and Elisa Maiques contributed equally to this work.

  • MaÁngeles Tormo,

    1. Centro de Investigación y Tecnología Animal, Instituto Valenciano de Investigaciones Agrarias (CITA-IVIA), Apdo. 187, 12.400 Segorbe, Castellón, Spain.
    2. Departamento de Química, Bioquímica y Biología Molecular, Universidad Cardenal Herrera-CEU, 46113 Moncada, Valencia, Spain.
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  • Susana Campoy,

    1. Centre de Recerca en Sanitat Animal (CReSA), 08193 Bellaterra, Spain.
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  • Íñigo Lasa,

    1. Instituto de Agrobiotecnología y Recursos Naturales, CSIC-Universidad Pública de Navarra, 31006 Pamplona, Navarra, Spain.
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  • Jordi Barbé,

    1. Departament de Genètica i Microbiologia, Universitat Autónoma de Barcelona, 08193 Bellaterra, Spain.
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  • Richard P. Novick,

    1. Skirball Institute, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA.
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  • José R. Penadés

    Corresponding author
    1. Centro de Investigación y Tecnología Animal, Instituto Valenciano de Investigaciones Agrarias (CITA-IVIA), Apdo. 187, 12.400 Segorbe, Castellón, Spain.
    2. Departamento de Química, Bioquímica y Biología Molecular, Universidad Cardenal Herrera-CEU, 46113 Moncada, Valencia, Spain.
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*E-mail jpenades@ivia.es; Tel. (+34) 96 34 24 007; Fax (+34) 96 34 24 001.

Summary

Transfer of Staphylococcus aureus pathogenicity islands (SaPIs) is directly controlled by the cellular repressor LexA. We have found that transcription of the SaPIbov1 operon I is repressed by LexA and is therefore SOS-induced. Two copies of the LexA binding site consensus (Cheo box) are present in the 5′ region of this operon, at the same location in all of 15 different SaPIs analysed. Both of these boxes bind LexA protein. Furthermore, replacement of the chromosomal lexA with a non-cleavable mutant LexA (G94E) greatly diminished expression of SaPIbov1 operon I and differentially reduced the production of SaPI transducing particles in comparison with the production of plaque-forming particles. In concordance with this finding, deletion of operon I blocked the formation of SaPI transducing particles but had no effect on replication of the island. Operon I contains a gene encoding a homologue of the phage terminase small subunit plus two other genes that direct the assembly of the small sized SaPIbov1 capsids. Interestingly, mutations affecting the latter two genes were not defective in SaPI transfer, but rather encapsidated the island in full-sized phage heads, which would have to contain a multimeric SaPI genome.

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