Control of Staphylococcus aureus pathogenicity island excision
Staphylococcus aureus pathogenicity islands (SaPIs) are a group of related 1517 kb mobile genetic elements that commonly carry genes for superantigen toxins and other virulence factors. The key feature of their mobility is the induction of SaPI excision and replication by certain phages and their ef...
| Autores principales: | , , , , , , , |
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| Formato: | Artículo |
| Lenguaje: | Inglés |
| Publicado: |
2017
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| Acceso en línea: | http://hdl.handle.net/20.500.11939/5635 |
| _version_ | 1855491958121693184 |
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| author | Mir, Ignacio Martinez-Rubio, Roser Marti, Miguel Chen, John Lasa, Inigo Novick, Richard P. Tormo-Mas, María A. Penadés, José R. |
| author_browse | Chen, John Lasa, Inigo Marti, Miguel Martinez-Rubio, Roser Mir, Ignacio Novick, Richard P. Penadés, José R. Tormo-Mas, María A. |
| author_facet | Mir, Ignacio Martinez-Rubio, Roser Marti, Miguel Chen, John Lasa, Inigo Novick, Richard P. Tormo-Mas, María A. Penadés, José R. |
| author_sort | Mir, Ignacio |
| collection | ReDivia |
| description | Staphylococcus aureus pathogenicity islands (SaPIs) are a group of related 1517 kb mobile genetic elements that commonly carry genes for superantigen toxins and other virulence factors. The key feature of their mobility is the induction of SaPI excision and replication by certain phages and their efficient encapsidation into specific small-headed phage-like infectious particles. Previous work demonstrated that chromosomal integration depends on the SaPI-encoded recombinase, Int. However, although involved in the process, Int alone was not sufficient to mediate efficient SaPI excision from chromosomal sites, and we expected that SaPI excision would involve an Xis function, which could be encoded by a helper phage or by the SaPI, itself. Here we report that the latter is the case. In vivo recombination assays with plasmids in Escherichia coli demonstrate that SaPI-coded Xis is absolutely required for recombination between the SaPI attL and attR sites, and that both sites, as well as their flanking SaPI sequences, are required for SaPI excision. Mutational analysis reveals that Xis is essential for efficient horizontal SaPI transfer to a recipient strain. Finally, we show that the master regulator of the SaPI life cycle, Stl, blocks expression of int and xis by binding to inverted repeats present in the promoter region, thus controlling SaPI excision. |
| format | Artículo |
| id | ReDivia5635 |
| institution | Instituto Valenciano de Investigaciones Agrarias (IVIA) |
| language | Inglés |
| publishDate | 2017 |
| publishDateRange | 2017 |
| publishDateSort | 2017 |
| record_format | dspace |
| spelling | ReDivia56352025-04-25T14:44:29Z Control of Staphylococcus aureus pathogenicity island excision Mir, Ignacio Martinez-Rubio, Roser Marti, Miguel Chen, John Lasa, Inigo Novick, Richard P. Tormo-Mas, María A. Penadés, José R. Staphylococcus aureus pathogenicity islands (SaPIs) are a group of related 1517 kb mobile genetic elements that commonly carry genes for superantigen toxins and other virulence factors. The key feature of their mobility is the induction of SaPI excision and replication by certain phages and their efficient encapsidation into specific small-headed phage-like infectious particles. Previous work demonstrated that chromosomal integration depends on the SaPI-encoded recombinase, Int. However, although involved in the process, Int alone was not sufficient to mediate efficient SaPI excision from chromosomal sites, and we expected that SaPI excision would involve an Xis function, which could be encoded by a helper phage or by the SaPI, itself. Here we report that the latter is the case. In vivo recombination assays with plasmids in Escherichia coli demonstrate that SaPI-coded Xis is absolutely required for recombination between the SaPI attL and attR sites, and that both sites, as well as their flanking SaPI sequences, are required for SaPI excision. Mutational analysis reveals that Xis is essential for efficient horizontal SaPI transfer to a recipient strain. Finally, we show that the master regulator of the SaPI life cycle, Stl, blocks expression of int and xis by binding to inverted repeats present in the promoter region, thus controlling SaPI excision. 2017-06-01T10:12:43Z 2017-06-01T10:12:43Z 2012 SEP 2012 article Mir-Sanchis, I., Martinez-Rubio, Roser, Marti, Miguel, Chen, John, Lasa, Inigo, Novick, Richard P., Angeles Tormo-Mas, M., Penades, J.R. (2012). Control of Staphylococcus aureus pathogenicity island excision. Molecular microbiology, 85(5), 833-845. 0950-382X http://hdl.handle.net/20.500.11939/5635 10.1111/j.1365-2958.2012.08145.x en openAccess Impreso |
| spellingShingle | Mir, Ignacio Martinez-Rubio, Roser Marti, Miguel Chen, John Lasa, Inigo Novick, Richard P. Tormo-Mas, María A. Penadés, José R. Control of Staphylococcus aureus pathogenicity island excision |
| title | Control of Staphylococcus aureus pathogenicity island excision |
| title_full | Control of Staphylococcus aureus pathogenicity island excision |
| title_fullStr | Control of Staphylococcus aureus pathogenicity island excision |
| title_full_unstemmed | Control of Staphylococcus aureus pathogenicity island excision |
| title_short | Control of Staphylococcus aureus pathogenicity island excision |
| title_sort | control of staphylococcus aureus pathogenicity island excision |
| url | http://hdl.handle.net/20.500.11939/5635 |
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