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Specificity of staphylococcal phage and SaPI DNA packaging as revealed by integrase and terminase mutations
Authors:Carles Ubeda  Nicholas P Olivarez  Peter Barry  Huaibin Wang  Xiangpeng Kong  Avery Matthews  Sandra M Tallent  Gail E Christie  Richard P Novick
Institution:Kimmel Center for Biology and Medicine, Skirball Institute, Program in Molecular Pathogenesis, and Departments of Microbiology and Biochemistry, New York University Medical Center, New York, NY 10016, USA.;
Department of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Richmond, VA 23298-0678, USA.;
Department of Biology, Virginia Commonwealth University Richmond, VA 23284-2012, USA.
Abstract:SaPI1 and SaPIbov1 are chromosomal pathogenicity islands in Staphylococcus aureus that carry tst and other superantigen genes. They are induced to excise and replicate by certain phages, are efficiently encapsidated in SaPI-specific small particles composed of phage virion proteins and are transferred at very high frequencies. In this study, we have analysed three SaPI genes that are important for the phage–SaPI interaction, int (integrase) terS (phage terminase small subunit homologue) and pif (phage interference function). SaPI1 int is required for SaPI excision, replication and packaging in a donor strain, and is required for integration in a recipient. A SaPI1 int mutant, following phage induction, produces small SaPI-specific capsids which are filled with partial phage genomes. SaPIbov1 DNA is efficiently packaged into full-sized phage heads as well as into SaPI-specific small ones, whereas SaPI1 DNA is found almost exclusively in the small capsids. TerS, however, determines DNA packaging specificity but not the choice of large versus small capsids. This choice is influenced by SaPIbov1 gene 12, which prevents phage DNA packaging into small capsids, and which is also primarily responsible for interference by SaPIbov1 with phage reproduction.
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