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

Úbeda, C., Maiques, E., Tormo, M., Campoy, S., Lasa, Í., Barbé, J., Novick, R.P. and Penades, J.R. (2007) SaPI operon I is required for SaPI packaging and is controlled by LexA. Molecular Microbiology, 65(1), pp. 41-50. (doi:10.1111/j.1365-2958.2007.05758.x)

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Abstract

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.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Penades, Professor Jose R
Authors: Úbeda, C., Maiques, E., Tormo, M., Campoy, S., Lasa, Í., Barbé, J., Novick, R.P., and Penades, J.R.
College/School:College of Medical Veterinary and Life Sciences > Institute of Infection Immunity and Inflammation
Journal Name:Molecular Microbiology
ISSN:0950-382X
ISSN (Online):1365-2958

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