Carles Úbeda and Elisa Maiques contributed equally to this work.
SaPI operon I is required for SaPI packaging and is controlled by LexA
Article first published online: 16 JUN 2007
Volume 65, Issue 1, pages 41–50, July 2007
How to Cite
Úbeda, C., Maiques, E., Tormo, M., Campoy, S., Lasa, Í., Barbé, J., Novick, R. P. and Penadés, J. R. (2007), SaPI operon I is required for SaPI packaging and is controlled by LexA. Molecular Microbiology, 65: 41–50. doi: 10.1111/j.1365-2958.2007.05758.x
- Issue published online: 16 JUN 2007
- Article first published online: 16 JUN 2007
- Accepted 23 April, 2007.
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.